Effect of degradation of a black mangrove forest on seasonal greenhouse gas emissions.

Mangroves play an essential role in the global carbon cycle. However, they are highly vulnerable to degradation with little-known effects on greenhouse gas (GHG) emissions. This study compared seasonal soil carbon dioxide (CO2), methane (CH4), and nitrous oxide (N2O) fluxes from a black mangrove (Avicennia germinans) forest in the Tampamachoco coastal lagoon, Veracruz, Mexico, in areas subjected to different degrees of environmental degradation (full canopy, transitional and dead mangrove), caused by hydrological perturbation. Furthermore, we aimed at determining the environmental factors driving seasonal fluxes. There was a combined effect of seasonality and degradation on CH4 fluxes, highest during the rainy season in the dead mangrove (0.93 ± 0.18 mg CH4 m-2 h-1). CO2 fluxes were highest during the dry season (220 ± 23 mg CO2 m-2 h-1), with no significant differences among degradation levels. N2O fluxes did not vary among seasons or degradation levels (- 3.8 to 2.9 mg N2O m-2 h-1). The overall CO2-eq emission rate was 15.3 ± 2.7 Mg CO2-eq ha-1 year-1, with CO2 as the main gas contributing to total emissions. The main factors controlling CH4 fluxes were seasonal porewater salinity and the availability of NO2-, NO3-, and SO4-2 in the soil, favored by high water level and temperature in the absence of pneumatophores. The main determining factors controlling CO2 fluxes were water level, porewater redox potential, and soil Cl- and SO4-2 concentration. Finally, N2O fluxes were related to NO2-, NO3-, and SO4-2 soil concentrations. This study contributes to improving the knowledge of soil GHG fluxes dynamics in mangroves and the effect of degradation of these ecosystems on the coastal biogeochemical cycles, which may bring important insights for assessing accurate ways to mitigate climate change protecting and restoring these ecosystems.

Melanoma of the sellar region mimicking pituitary adenoma.

We report here the case of an 82-year-old woman who presented with visual disturbance. MRI demonstrated a sellar mass. The diagnosis of pituitary adenoma was made. She underwent transnasal surgery. Histologic, immunohistochemical and ultrastructural studies indicated that the tumor was a melanoma. Despite an exhaustive search for a primary lesion elsewhere, none was found. The sellar tumor was considered a primary lesion, although extrasellar primary tumor imaging cannot be excluded with 100% certainty. Reported examples of melanoma affecting the sellar region are few. They exhibit morphologic features identical to those of melanomas arising elsewhere. Although very rare, primary melanomas enter into the differential diagnosis of sellar lesions.

Temozolomide in aggressive pituitary adenomas and carcinomas.

Temozolomide is an alkylating agent used in the treatment of gliomas and, more recently, aggressive pituitary adenomas and carcinomas. Temozolomide methylates DNA and, thereby, has antitumor effects. O6-methylguanine-DNA methyltransferase, a DNA repair enzyme, removes the alkylating adducts that are induced by temozolomide, thereby counteracting its effects. A Medline search for all of the available publications regarding the use of temozolomide for the treatment of pituitary tumors was performed. To date, 46 cases of adenohypophysial tumors that were treated with temozolomide, including 30 adenomas and 16 carcinomas, have been reported. Eighteen of the 30 (60%) adenomas and 11 of the 16 (69%) carcinomas responded favorably to treatment. One patient with multiple endocrine neoplasia type 1 and an aggressive prolactin-producing adenoma was also treated and demonstrated a good response. No significant complications have been attributed to temozolomide therapy. Thus, temozolomide is an effective treatment for the majority of aggressive adenomas and carcinomas. Evidence indicates that there is an inverse correlation between levels of O6-methylguanine-DNA methyltransferase immunoexpression and therapeutic response. Alternatively, high-level O6-methylguanine-DNA methyltransferase immunoexpression correlates with an unfavorable response. Here, we review the use of temozolomide for treating pituitary neoplasms.

Pituitary tumors in patients with MEN1 syndrome.

We briefly review the characteristics of pituitary tumors associated with multiple endocrine neoplasia type 1. Multiple endocrine neoplasia type 1 is an autosomal-dominant disorder most commonly characterized by tumors of the pituitary, parathyroid, endocrine-gastrointestinal tract, and pancreas. A MEDLINE search for all available publications regarding multiple endocrine neoplasia type 1 and pituitary adenomas was undertaken. The prevalence of pituitary tumors in multiple endocrine neoplasia type 1 may vary from 10% to 60% depending on the studied series, and such tumors may occur as the first clinical manifestation of multiple endocrine neoplasia type 1 in 25% of sporadic and 10% of familial cases. Patients were younger and the time between initial and subsequent multiple endocrine neoplasia type 1 endocrine lesions was significantly longer when pituitary disease was the initial manifestation of multiple endocrine neoplasia type 1. Tumors were larger and more invasive and clinical manifestations related to the size of the pituitary adenoma were significantly more frequent in patients with multiple endocrine neoplasia type 1 than in subjects with non-multiple endocrine neoplasia type 1. Normalization of pituitary hypersecretion was much less frequent in patients with multiple endocrine neoplasia type 1 than in subjects with non-multiple endocrine neoplasia type 1. Pituitary tumors in patients with multiple endocrine neoplasia type 1 syndrome tend to be larger, invasive and more symptomatic, and they tend to occur in younger patients when they are the initial presentation of multiple endocrine neoplasia type 1.

Anti-VEGF therapy in pituitary carcinoma.

We report the case of a 44-year-old male patient with an aggressive silent corticotroph cell pituitary adenoma, subtype 2. In that it progressed to carcinoma despite temozolomide administration, anti-VEGF therapy was begun. MRI, PET scan and pathologic analysis were undertaken. After 10 months of anti-VEGF (bevacizumab) treatment no progression of the lesion was noted. The tumor was biopsied and morphological analysis showed severe cell injury, vascular abnormalities and fibrosis. Bevacizumab treatment has continued for additional 16 months to present with stabilization of disease as documented on serial MRI and PET scans. This is the first case of a bevacizumab-treated pituitary carcinoma with long-term, now 26 months, control of disease. The present findings are promising in that anti-angiogenic therapy appears to represent a new option in the treatment of aggressive pituitary tumors.

Neurocysticercosis, meningioma, and silent corticotroph pituitary adenoma in a 61-year-old woman.

We report here the case of a 61-year-old woman who presented with hydrocephalus and cystic and solid lesions in sella turcica, suprasellar areas, and third ventricle. After ventriculoperitoneal shunt she developed cognitive changes and the cystic lesions enlarged. Magnetic resonance imaging (MRI) demonstrated multiple cysts and a solid lesion in the sella and around the anterior clinoid process. With diagnosis of neurocysticercosis she underwent craniotomy. Pathologic examination documented two different lesions: viable and dead cysticerci with inflaming infiltration and a left anterior clinoidal meningioma. At the second surgery, six weeks later via transnasal transsphenoidal approach a silent corticotroph pituitary adenoma was removed which was studied by histology, immunohistochemistry, and electron microscopy. To our knowledge, the occurrence of these three different lesions in the sellar area was not described before.

Somatotroph pituitary adenoma with acromegaly and autosomal dominant polycystic kidney disease: SSTR5 polymorphism and PKD1 mutation.

A 39-year-old woman with autosomal dominant polycystic kidney disease (ADPKD) presented with acromegaly and a pituitary macroadenoma. There was a family history of this renal disorder. She had undergone surgery for pituitary adenoma 6 years prior. Physical examination disclosed bitemporal hemianopsia and elevation of both basal growth hormone (GH) 106 ng/mL (normal 0-5) and insulin-like growth factor (IGF-1) 811 ng/mL (normal 48-255) blood levels. A magnetic resonance imaging scan disclosed a 3.0 cm sellar and suprasellar mass with both optic chiasm compression and left cavernous sinus invasion. Pathologic, cytogenetic, molecular and in silico analysis was undertaken. Histologic, immunohistochemical and ultrastructural studies of the lesion disclosed a sparsely granulated somatotroph adenoma. Standard chromosome analysis on the blood sample showed no abnormality. Sequence analysis of the coding regions of PKD1 and PKD2 employing DNA from both peripheral leukocytes and the tumor revealed the most common PKD1 mutation, 5014_5015delAG. Analysis of the entire SSTR5 gene disclosed the variant c.142C>A (p.L48M, rs4988483) in the heterozygous state in both blood and tumor, while no pathogenic mutations were noted in the MEN1, AIP, p27Kip1 and SSTR2 genes. To our knowledge, this is the fourth reported case of a GH-producing pituitary adenoma associated with ADPKD, but the first subjected to extensive morphological, ultrastructural, cytogenetic and molecular studies. The physical proximity of the PKD1 and SSTR5 genes on chromosome 16 suggests a causal relationship between ADPKD and somatotroph adenoma.

Pituitary tumors in patients with MEN1 syndrome

We briefly review the characteristics of pituitary tumors associated with multiple endocrine neoplasia type 1. Multiple endocrine neoplasia type 1 is an autosomal-dominant disorder most commonly characterized by tumors of the pituitary, parathyroid, endocrine-gastrointestinal tract, and pancreas. A MEDLINE search for all available publications regarding multiple endocrine neoplasia type 1 and pituitary adenomas was undertaken. The prevalence of pituitary tumors in multiple endocrine neoplasia type 1 may vary from 10% to 60% depending on the studied series, and such tumors may occur as the first clinical manifestation of multiple endocrine neoplasia type 1 in 25% of sporadic and 10% of familial cases. Patients were younger and the time between initial and subsequent multiple endocrine neoplasia type 1 endocrine lesions was significantly longer when pituitary disease was the initial manifestation of multiple endocrine neoplasia type 1. Tumors were larger and more invasive and clinical manifestations related to the size of the pituitary adenoma were significantly more frequent in patients with multiple endocrine neoplasia type 1 than in subjects with non-multiple endocrine neoplasia type 1. Normalization of pituitary hypersecretion was much less frequent in patients with multiple endocrine neoplasia type 1 than in subjects with non-multiple endocrine neoplasia type 1. Pituitary tumors in patients with multiple endocrine neoplasia type 1 syndrome tend to be larger, invasive and more symptomatic, and they tend to occur in younger patients when they are the initial presentation of multiple endocrine neoplasia type 1.

Temozolomide in aggressive pituitary adenomas and carcinomas

Temozolomide is an alkylating agent used in the treatment of gliomas and, more recently, aggressive pituitary adenomas and carcinomas. Temozolomide methylates DNA and, thereby, has antitumor effects. O6-methylguanine-DNA methyltransferase, a DNA repair enzyme, removes the alkylating adducts that are induced by temozolomide, thereby counteracting its effects. A Medline search for all of the available publications regarding the use of temozolomide for the treatment of pituitary tumors was performed. To date, 46 cases of adenohypophysial tumors that were treated with temozolomide, including 30 adenomas and 16 carcinomas, have been reported. Eighteen of the 30 (60%) adenomas and 11 of the 16 (69%) carcinomas responded favorably to treatment. One patient with multiple endocrine neoplasia type 1 and an aggressive prolactin-producing adenoma was also treated and demonstrated a good response. No significant complications have been attributed to temozolomide therapy. Thus, temozolomide is an effective treatment for the majority of aggressive adenomas and carcinomas. Evidence indicates that there is an inverse correlation between levels of O6-methylguanine-DNA methyltransferase immunoexpression and therapeutic response. Alternatively, high-level O6-methylguanine-DNA methyltransferase immunoexpression correlates with an unfavorable response. Here, we review the use of temozolomide for treating pituitary neoplasms.

Aggressive silent corticotroph adenoma progressing to pituitary carcinoma: the role of temozolomide therapy.

Temozolomide (TMZ) has recently been recommended as a novel approach in the management of aggressive pituitary tumors. Herein, we present the case of a 43-year-old man with a 20-year history of silent subtype 2 pituitary corticotroph adenoma. Nine surgical resections and radiotherapy had failed to provide a cure. Morphological evaluation of the tumor revealed a mildly pleomorphic adenoma, the cells of which showed low-level cell proliferative activity with Ki67, increased topoisomerase II alpha index and conclusive O-6-methylguanine-DNA methyltransferase (MGMT) as well as vascular endothelial growth factor (VEGF) immunoreactivity. Given its aggressive behavior and failure of conventional therapy, TMZ was administered. The treatment was continued even after MGMT immunopositivity was identified, but failed to decrease MGMT immunoexpression and exerted no morphologic effect. Examination of the lesion after TMZ therapy showed neither morphologic nor immunohistochemical alterations. In our case, TMZ administration, despite changing the TMZ dosing regimen to prompt a drug response, was incapable of depleting MGMT stores.

Treatment of pituitary neoplasms with temozolomide: a review.

Temozolomide, an orally administered alkylating agent, is used to treat malignant gliomas. Recent reports also have documented its efficacy in the treatment of pituitary adenomas and carcinomas. Temozolomide methylates DNA and thereby exhibits an antitumor effect. O6-methylguanine-DNA methyltransferase (MGMT), a DNA repair enzyme, removes alkylating adducts induced by temozolomide, counteracting its effects. The authors of this review conducted a Medline database search regarding temozolomide in the treatment of pituitary tumors. Demographic characteristics, tumor types, and therapeutic responses were noted in all patients. Data regarding MGMT immunoexpression, which was documented in some studies, were correlated with information regarding clinical and radiologic responses. To date, there have been 19 reported cases of adenohypophyseal tumors treated with temozolomide, including 13 adenomas and 6 carcinomas. Ten of those 13 adenomas responded favorably, and 2 nonresponsive tumors had high-level MGMT immunoexpression. All 6 carcinomas responded to therapy, but data regarding MGMT expression were available for only 3 patients, and each had low MGMT expression. In 2 adenomas, morphologic studies were performed both before and after the patients received temozolomide. The responsive tumor had necrosis, hemorrhage, fibrosis, and neuronal differentiation. The nonresponsive tumor had no changes. There have been no reported complications attributable to temozolomide. The current results indicated that temozolomide is efficacious in the treatment of aggressive pituitary adenomas and pituitary carcinomas. Evidence indicated that low-level MGMT immunoexpression is correlated with a favorable response. A significant proportion of pituitary adenomas and carcinomas had low MGMT immunoexpression.

Pituitary adenoma with peliosis: a report of two cases.

Peliosis is characterised by multiple blood-filled lakes or cavities within parenchymatous organs. Typically found in the liver, spleen, bone marrow and lymph nodes, it has also been described in other organs such as lungs, kidneys, parathyroids and pancreas. The mechanism responsible for the development of peliosis remains unknown. (1) A 69 year-old man with a 6-year history of acromegaly underwent transsphenoidal surgery for pituitary adenoma. Morphologic findings demonstrated a plurimorphous plurihormonal pituitary adenoma consisting of somatotrophs, lactotrophs and mammosomatotrophs. The tumor contained several blood-filled cavities characteristic of peliosis. (2) A 61-year-old man with a prolactin-producing pituitary adenoma who underwent transsphenoidal surgery. In the tumor, peliosis was noted. Peliosis in a pituitary adenoma is an intriguing finding. The question arises whether it represents vasculogenic mimicry.

Temozolomide therapy in a man with an aggressive prolactin-secreting pituitary neoplasm: Morphological findings.

Administration of temozolomide to a 46-year-old man with an invasive aggressive prolactin (PRL)-secreting pituitary neoplasm resulted in improvement of the clinical condition and significant decrease of blood PRL levels. Histologic, immunohistochemical, and electron microscopic study demonstrated marked morphological differences in the tumor exposed to temozolomide compared with the unexposed tumor. Necrosis, hemorrhagic areas, accumulation of connective tissue, focal inflammatory infiltration, and neuronal transformation were seen. Immunohistochemical prognostic indicators showed a reduction in growth potential. Based on the clinical, laboratory, and morphological findings, we recommend temozolomide therapy in patients with pituitary tumors not responding adequately to other treatment options.

Plurihormonality in pituitary adenomas associated with acromegaly.

Bihormonal or plurihormonal pituitary tumors produce two or more hormones different in chemical composition, immunoreactivity, and clinical significance. Immunohistochemical and electron microscopic investigations and more recently molecular-genetic studies have provided conclusive evidence of the production of multiple hormones by pituitary adenomas. Most frequently, they produce GH, PRL, TSH, and/or alpha-subunit of the glycoprotein hormones. Other uncommon combinations may also be apparent. We report the case of a 40-yr-old acromegalic man with a pituitary macroadenoma. The pituitary tumor was removed by transsphenoidal surgery. Histological, immunohistochemical, electron microscopic, and immunoelectron microscopic examinations revealed that the tumor contains multiple hormones (GH, LH, and alpha subunit) and transcription factors. The application of different reagents yielded different patterns of positivity indicating that the validity of some common immunohistochemical reagents must be re-evaluated.

Inflammatory pseudotumor of the pituitary: case report.

BACKGROUND: Inflammatory pseudotumor of the pituitary is a very rare nonneoplastic lesion. We describe a case of a patient with past history of lymphocytic meningitis. CASE DESCRIPTION: A 32-year-old man presented with polyuria, polydipsia, anorexia, abdominal discomfort, and panhypopituitarism. He had 2 episodes of lymphocytic meningitis in the last two years. Magnetic resonance image (MRI) disclosed a sellar and suprasellar mass with extension to the pituitary stalk. The patient underwent transnasal-transsphenoidal surgery to remove the lesion. Histopathological findings revealed mixed inflammatory cells composed mainly of lymphocytes, macrophages and extensive fibrosis. CONCLUSIONS: Inflammatory pseudotumor of the pituitary, although rare, should be included in the differential diagnosis of a sellar and suprasellar mass.

Prolactin-producing pituitary adenoma associated with prolactin cell hyperplasia.

A 24-yr-old woman with amenorrhea, galactorrhea, hyperprolactinemia, and sellar mass underwent transsphenoidal surgery. Histologic, immunohistochemical, and electron microscopic investigation revealed a well-differentiated, sparsely granulated prolactin (PRL) cell adenoma of the pituitary showing conclusive PRL immunoreactivity. In the nontumorous adenohypophysis PRL cell hyperplasia was noted. Marked differences were evident between the neoplastic and hyperplastic areas. The tumor consisted of sparsely granulated PRL cells immunoreactive only for PRL. As demonstrated by immunoelectron microscopy, the hyperplastic area comprised monohormonal sparsely granulated PRL cells as well as bihormonal mammosomatotrophs immunoreactive for both PRL and growth hormone. The MIB-1 index was higher whereas microvessel density was lower in the adenoma as compared with the hyperplastic area. In addition, the nontumorous area showed lymphocytic infiltration whereas inflammatory reaction was not seen in the adenoma. This case represents a rare association of a PRL cell adenoma and PRL cell hyperplasia. The fact that these two lesions were contiguous in the surgically removed material raises the possibility that hyperplasia can precede and transform into adenoma.