Fat necrosis may mimic local recurrence of breast cancer in FDG PET/CT / La necrosis grasa puede asemejarse a una recurrencia local del cáncer de mama en la PET/TC con FDG

Fat necrosis of the breast is a benign condition that most commonly occurs as the result of trauma. The radiographic and clinical significance of fat necrosis of the breast is that it may mimic malignancy. We present a case of false positive FDG PET/CT scan caused by fat necrosis and mimics local recurrence of breast carcinoma 3 years after radical mastectomy. Physicians must be aware of fat necrosis as a potential pitfall for PET/CT. Fat necrosis must be considered in the differential diagnosis of hypermetabolic breast masses in patients who previously had mastectomy or mammoplasty (AU)

La necrosis grasa de mama constituye una situación benigna que se produce de forma común como resultado de un trauma. El significado radiográfico y clínico de la necrosis grasa puede asemejarse a una neoplasia. Presentamos el caso de un resultado falso positivo de la PET/TC con FDG debido a una necrosis grasa, y su semejanza con una recurrencia local de carcinoma de mama a los 3 años de una mastectomía radical. Los facultativos deben ser conscientes de que la necrosis grasa puede constituir una limitación para el estudio PET/TC. La necrosis grasa debe considerarse en el diagnóstico diferencial de las masas hipermetabólicas de mama en pacientes sometidas previamente a mastectomía o mamoplastia (AU)

Ischaemic time and fat necrosis in breast reconstruction with a free deep inferior epigastric perforator flap.

PURPOSE: Fat tissue can be injured by ischaemia in free flap surgeries, leading to the development of fat necrosis. The aim of this study was to evaluate the association between ischaemic time and fat necrosis in microsurgical breast reconstruction using a deep inferior epigastric perforator (DIEP) flap. METHODS: A retrospective chart review was performed for patients who underwent breast reconstruction with free DIEP flaps between June 2009 and November 2011. Data regarding patient demographics, potential risk factors and fat necrosis were collected. Fat necrosis was diagnosed with ultrasound imaging between 3 and 6 months postoperatively. Univariate and multivariate analyses were used to assess the correlation between ischaemic time and fat necrosis rate. Receiver operating characteristic curve analysis was used to determine a cut-off value for the ischaemic time at which differential fat necrosis rates were maximal. RESULTS: A total of 86 patients were included in this study. The mean ischaemic time was 89 min, and fat necrosis was diagnosed in 15 patients (17.4%). A significant association was found between ischaemic time and fat necrosis rate on univariate (p-value=0.001) and multivariate analyses (p-value=0.017). The trend analysis of ischaemic time as a categorical variable relative to fat necrosis rate was also significant (p-value<0.001). A threshold value was found whereby patients with an ischaemic time longer than 99.5 min appeared to experience a significantly higher fat necrosis rate than patients with shorter times (p-value=0.005, odds ratio=9.449). CONCLUSION: Ischaemic time appears to be significantly associated with increased fat necrosis rate in breast reconstruction using DIEP flaps. A long ischaemia time may be a risk factor for the development of fat necrosis.

Subcutaneous fat necrosis: a complication of neuroprotective cooling.

Because neuroprotective cooling for hypoxic ischemic encephalopathy (HIE ) becomes more commonplace in NICU s, health care providers should be familiar with the complications of this therapy. Therapeutic cooling improves neurodevelopmental outcomes and has relatively few side effects. One unexpected outcome that has been reported is subcutaneous fat necrosis (SCFN). This column describes the problem, and recommends that NICU staff be vigilant in their observation for, as well as timely in their interventions to help prevent SCFN.

Reduction mammoplasty with superolateral dermoglandular pedicle: details of 15 years of experience.

The techniques of reduction mammoplasty are multiple and varied. Each one has advantages and disadvantages. With any of them, full preservation of vascularity and sensitizing of the nipple-areola complex (NAC) should be sought, as well as functionality of the breast. We present our 15 years' experience using the superolateral dermoglandular pedicle, a technique that fully preserves the integrity of the breast. During that 15-year period, we operated on 702 breasts in 356 patients, using the superolateral dermoglandular pedicle, with the NAC requiring a migration of 5 to 16 cm (mean: 9.2 cm), having resected breast tissue between 300 and 1380 g, (average: 660 g). The technique was used in women between 16 and 63 years of age (average 37), who wanted breast reduction and who required a migration of the NAC greater than 5 cm. We had minor complications consisting of wound dehiscence (5.9%), scar hyperpigmentation (3.9%), fat necrosis (3.8%), hypertrophic scarring (3.1%), alterations in sensitivity (2.27%), and keloid scarring (0.5%). We had 9 cases of necrosis of the NAC (1.28%), of which 7 were partial (0.99%) and 2 were total (0.28%). Satisfaction with the results was 94%. The technique of reduction mammoplasty with a superolateral dermoglandular pedicle has been used in mammary hypertrophy and gigantomasty with excellent results. Its design is simple, its performance easy, and its aesthetic results are highly reproducible. The position of the pedicle allows full preservation of the vascularity, sensitivity, and functionality of the breast, and is therefore a highly recommendable technique.

Esteatohepatitis no alcohólica: fisiopatogenia y modelos experimentales / Nonalcoholic esteatohepatitis. Physopathogeny and experimental models

Se hizo una revisión sobre la esteatohepatitis no alcohólica, la cual durante años fue considerada una enfermedad poco común y de buen pronóstico. Sin embargo, el conocimiento de que entre 15 y 50 por ciento de los pacientes presentan fibrosis y hasta cirrosis en sus biopsias, hizo que cambiara esa percepción, y en estos momentos es una de las entidades a las que más atención se le está prestando dentro del campo de la Hepatología. A pesar de que la fisiopatogenia de esta entidad es compleja y no bien elucidada aún, la teoría de los 2 hits, propuesta en 1998, explica los principales mecanismos fisiopatogénicos implicados en su desarrollo. Existen varios modelos experimentales para el estudio de la esteatohepatitis no alcohólica. No obstante, el modelo animal que reproduce con mayor fidelidad la fisiopatogenia de la esteatohepatitis no alcohólica es el logrado por Lieber y otros a partir del empleo en ratas de una dieta líquida rica en grasas(AU)

Nódulos subcutáneos en un recién nacido / Subcutaneous nodules in a newborn

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Oxidized LDL-induced injury and apoptosis in atherosclerosis. Potential roles for oxysterols.

The cell injury caused by oxidized lipoproteins was among the first findings that led to the theory that it is the oxidation of low-density lipoprotein (LDL), not just LDL concentration, that leads to arterial disease. Voluminous studies have now revealed that oxidized lipoproteins and their constituents can induce numerous effects on cells that can be construed to be atherogenic. Cell injury is but one of these, and it is these injurious effects that are the focus of this brief review. Cell injury and death appear to play multiple roles in lesion development and the toxic lipid constituents of oxidized lipoproteins, including a variety of oxysterols, are candidates for the in vivo effectors of this cytotoxicity. Recent studies have focused on the mechanisms of oxidized lipoprotein-induced cell death, whether the cells die by apoptosis or necrosis, and the identities of the toxins that induce injury. Understanding the roles of these agents in lesion development could lead to therapies that modulate cell death and inhibit lesion formation.

[Perinatal maternal emergencies]. / Urgences maternelles périnatales.

The perinatal period (from the 28th week of pregnancy to the 28th day after delivery) is a short but special period which endangers the mother's and child's life. There has been no elective statistical assessment of this period but surveys conducted in western countries show that most of the maternal emergencies requiring admission to an intensive care unit are actually those of the perinatal period; some are specific of pregnancy: gravidic toxemia, delivery hemorrhage, acute fatty liver of pregnancy; others such as septic or embolic shock, cardiomyopathy, are found also in non-pregnant women but are favored by pregnancy. Among the numerous eventualities it was necessary to take a selection: ours results from three sorts of considerations: i) the severity of some of these perinatal emergencies: preeclampsia, eclampsia, Hellp syndrome, subcapsula hepatic rupture, septic or hemorrhagic shock are among the most serious ones; ii) the high frequency of some of them: post partum hemorrhage is, in France, the first cause of maternal mortality and the second cause of maternal morbidity whereas infection which can bring a septic shock is found to complicate one to eight per cent of the deliveries; iii) several emergency conditions raise pathophysiological problems which are still not entirely solved, for instance, gravidic toxemia, acute fatty liver of pregnancy, amniotic embolism. They will be especially studied here. Maternal perinatal emergencies remain a major public health problem. It is a necessity to realize the importance of the stakes, to encourage a team spirit, to combine the abilities of obstetricians, intensive care physicians, anaesthesists, echographists, biologists, so that this race against time can be won.

Regression of hepatic steatosis in morbidly obese persons after gastric bypass.

Morbid obesity has been associated with hepatic steatosis and occasional cirrhosis. Despite producing weight loss, intestinal bypass procedures formerly performed to correct morbid obesity, often worsened steatosis and fibrosis, and occasionally resulted in hepatic failure. Current surgical procedures of choice for morbid obesity involve gastric bypass with gastrojejunostomy. Ninety-one liver biopsies taken at the time of gastric bypass for morbid obesity (mean body weight 125.8 kg), and 106 biopsies taken from the same patients from 2 to 61 months later (mean body weight 89.4 kg) were studied. Steatosis and perisinusoidal fibrosis were assessed in histologic sections. Serum albumin, alkaline phosphatase, aspartate aminotransferase (AST), and total bilirubin levels were measured before most biopsies were taken. Both pre- and post-gastric bypass hepatic steatosis varied directly with body weight (r = .5231, P < .001). Steatosis varied inversely with length of time after gastric bypass (r = .4590, P < .001). Of the original biopsies, 37% had lipid vacuoles in at least 26% of hepatocytes. After gastric bypass, 65 patients had reduced steatosis, 18 patients with no steatosis, and 5 patients with minimal steatosis had no change, and 3 patients had increased steatosis. Pre-gastric bypass biopsies from 13 patients had perisinusoidal fibrosis (PSF) that was marked with bridging in three patients, was moderate in one patient, and slight in nine patients. Following gastric bypass, PSF was eliminated in 10 patients, reduced in one patient, and the same in two patients. One patient developed PSF after gastric bypass. Of the three patients who had undergone previous intestinal bypass procedures, two had slight PSF in the biopsies taken at the time of gastric bypass, and one of these had slight PSF in the follow-up biopsy. Serum biochemical abnormalities tended to be slight. Before gastric bypass, serum albumin was low in 11% of cases, alkaline phosphatase was high in 14% of cases, AST was high in 11% of cases, and total bilirubin was high in 1% of cases. After gastric bypass, there was a small reduction in mean serum albumin from 43 g/L before to 41 g/L afterward (P < .05), and a slight rise in mean total bilirubin from 7.0 mumol/L before to 9.6 mu mol/L afterward (P < .01). Most hepatic fatty change and probably some PSF occurring in morbidly obese persons is reduced or eliminated with weight loss following gastric bypass surgery.

Subcutaneous fat necrosis in a neonate, in association with aberrant plasma lipid and lipoprotein values.

A newborn infant with subcutaneous fat necrosis after perinatal hypoxia was found to have several abnormalities of plasma lipids. Further studies are needed to determine whether such abnormalities contribute to the pathophysiology of the skin lesions.

Pancreatic-portal vein fistula with disseminated fat necrosis treated by pancreaticoduodenectomy.

I have reported the case of a 62-year-old man with chronic alcoholic pancreatitis and a rare pseudocyst-portal vein fistula. Even though he experienced no abdominal symptoms, he had severe metastatic fat necrosis manifested as subcutaneous fat necrosis, polyarthritis, medullary bone necrosis, and mental status changes. Remote tissue destruction continued until relief was gained by pancreaticoduodenectomy and repair of the necrotic portal vein. Disseminated fat necrosis is a rare syndrome that can be the only presenting feature in patients with pancreatitis and pancreatic cancer. Early recognition and treatment of the underlying pancreatic disease may decrease the high morality rate associated with this syndrome.

Subcapsular steatonecrosis in response to peritoneal insulin delivery: a clue to the pathogenesis of steatonecrosis in obesity.

Hepatic steatosis and steatonecrosis occur in nonalcoholic individuals, usually in a setting of obesity, type II diabetes mellitus, and after jejunoileal bypass. We propose an hypothesis for the pathogenesis of these hepatic lesions based on an observation in peritoneal dialysis patients. Hepatic histology was examined at autopsy in 11 patients with type I diabetes mellitus and renal failure who had received i.p. insulin in conjunction with continuous ambulatory peritoneal dialysis (CAPD). Steatosis in a unique subcapsular distribution occurred in 10 of 11 patients treated with i.p. insulin and in 0 of 9 controls receiving CAPD without insulin. Three of the 11 had steatonecrosis, 2 of whom had Mallory bodies. We suggest that insulin has an important role in the pathogenesis of steatosis and steatonecrosis. In CAPD patients the lesions occurred only under the capsule where concentrations of insulin are high secondary to its i.p. administration. In obese patients the lesions occur throughout the liver where insulin concentrations are high because of elevated levels in the portal vein. Free fatty acids (FFA) are oxidized in the liver by a pathway that is blocked by insulin. In the presence of insulin, FFA are preferentially esterified into triglycerides which accumulate in large quantities leading to steatosis; small amounts of FFA escaping local control may lead to membrane injury and steatonecrosis. Steatosis and/or steatonecrosis will occur when there is insulin secretion sufficient to block FFA oxidation but not sufficient to block FFA mobilization from adipose tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

[3 cases of neonatal cyto-steatonecrosis. Physiopathological discussion]. / Trois cas de cytostéatonécrose néo-natale. Discussion physiopathologique.

Three cases of subcutaneous fat necrosis of the newborn (SFNN) are presented. They occurred after a therapeutic coma induced by intravenous barbiturates to control convulsions unresponsive to conventional treatment. Two patients had widespread lesions. Histopathology showed prominent vascular involvement. Since 1970, 26 cases of SFNN have been published. Among the aetiological factors already described, hypothermia and ischaemia play a major role. It is suggested that brown adipose tissue might be of importance in the pathophysiology of subdural fat necrosis of the newborn.