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Oliver Gimm

Publications and source records attributed to Oliver Gimm.

At least 37 records · Page 2Linked to original sources
PubMed2005

The expression of CD97EGF and its ligand CD55 on marginal epithelium is related to higher stage and depth of tumor invasion of gastric carcinomas.

CD97EGF is a member of the EGF-TM7 family of class II seven-transmembrane (7TM), and its cellular ligand CD55 (also known as decay accelerating factor; DAF) protects host cells from complement attack. To determine whether the expression levels of these two molecules are correlated with the clinicopathological features of gastric carcinomas, a total of 35 gastric carcinomas and their corresponding margins and normal specimens were investigated by RT-PCR, Western blot analysis and immunohistochemistry. Transcript levels of CD97EGFand CD55 were higher in tumors than those in the margin and normal epithelial mucous tissues (P<0.05). However, the expression levels of CD97EGF and CD55 mRNA had no correlation with the clinicopathological features of gastric carcinoma patients. All three groups of specimens were immunoreactive for CD97EGF and the CD55 protein. Strong and specific immunoreactivities of CD97EGF were located in the mucosal epithelia of the marginal basal membrane. Expression of CD97(EGF) in the margins showed a marked difference between the depth of tumor invasion T1 and T2, 3 and 4, and stages I and II/III/IV of gastric carcinomas (P<0.05). The expression of CD55 protein was highly correlated with CD97EGF (R=0.6483, P<0.001). Western blot analysis confirmed the expression and distribution patterns of CD97EGF and CD55. Our findings suggest that CD97EGF may play a role in the development and invasion of gastric carcinomas by binding its cellular ligand CD55. Detection of the CD97EGF expression in the tumor margin could be referred to as the molecular edge of gastric carcinomas.

Antigens, CD↗
PubMed2004

Surgery of resectable nonfunctioning neuroendocrine pancreatic tumors.

Nonfunctioning neuroendocrine pancreatic tumors (NFNEPTs) comprise about one-third of pancreatic endocrine tumors. Based on immunohistochemistry, nonfunctioning tumors are difficult to distinguish from functioning ones; therefore the final diagnosis is basically the result of a synopsis of pathology and clinical data. Owing to their incapacity to produce hormone-dependent symptoms, NFNEPTs are detected incidentally or because of uncharacteristic symptoms resulting from local or distant growth. About two-thirds of NFNEPTs are located in the pancreatic head, so jaundice may be a late symptom of this tumor. Modern diagnostic procedures are best applied by a stepwise approach: first endoscopic ultrasonography and computed tomography/magnetic resonance imaging followed by somatostatin receptor scintigraphy or positron emission tomography (or both). Due to significant false-positive and false-negative findings, for decision-making the latter should be confirmed by a second imaging modality. Regarding indications for surgery and the surgical approach to the pancreas, three pancreatic manifestations of NFNEPTs can be distinguished: (1) solitary benign non-multiple endocrine neoplasia type 1 (non-MEN-1); (2) multiple benign MEN-1; and (3) malignant NFNEPTs. Reviewing the literature and including our experience with 18 NFNEPTs (8 benign, 10 malignant) reported here, the following conclusions can be drawn: (1) Solitary benign non-MEN-1 NFNEPTs can be removed by enucleation or by pancreas-, spleen-, and duodenum-preserving techniques in most cases. The choice of surgical technique depends on the location and site of the tumor and its anatomic relation to the pancreatic duct. (2) With multiple benign MEN-1 NFNEPTs, because of the characteristics of the underlying disease a preferred, more conservative concept (removal of only macrolesions) competes with a more radical procedure (left pancreatic resection with enucleation of head macrolesions). Further studies are necessary to clarify the best way to balance quality of life (by preserving organ function) with growth control of potentially malignant tumors in the pancreas. (3) Malignant NFNEPTs comprise more than half of all NFNEPTs. Few studies have analyzed treatment strategies for localized or metastatic tumors. Whereas radical (including multivisceral) resection of tumors without distant metastases is widely accepted, the indication for radical surgery on metastasizing tumors has been questioned, as radical removal of the primary tumor may fail to increase survival. Adjuvant regimens in these tumor stages are mandatory and should be further optimized.

Carcinoma, Neuroendocrine↗
PubMed2004

Single center experience in primary surgery for medullary thyroid carcinoma.

Medullary thyroid carcinoma (MTC) is a rare disease, and most studies are either based on small numbers or multicenter studies with their inherent difficulties. Since 1995, a total of 440 patients with MTC underwent surgery in our clinic. A primary operation was performed in 188 patients (43% of 440). In 60 patients, the primary operation was performed because of a germline RET mutation ("prophylactic surgery"). Most (84%, 158/188) of the patients had pathologic calcitonin levels. Notably, MTC was found in almost 10% (3/30) of patients with normal calcitonin levels. However, all patients with lymph node metastases (LNMs) had elevated calcitonin levels. Total thyroidectomy (TTx) was performed in all patients. Lymph node dissection (LND) was performed at various extensions: one-compartment LND in 35% (66/188), three-compartment LND in 31% (58/188), and four-compartment LND in 29% (22/188). In general, lymph node dissection increased the likelihood of complications. LNM and distant metastases (DM) correlated with the extent of the primary tumor (pT category). The presence of LNM ranged from 17% (pT1 tumor) to 100% (pT4 tumor), whereas the presence of DM ranged from 0% (pT1 tumor) to 81% (pT4 tumor). Biochemical cure (normal calcitonin levels) was obtained in 72% (137/188) of patients. All 60 patients undergoing prophylactic surgery (tumor stage pT0/pT1) were biochemically cured. In contrast, only 60% (77/128) of the remaining patients were cured. The data suggest that primary surgery should be scheduled as soon as possible to treat patients at a node-negative stage. In the case of normal basal and elevated stimulated calcitonin levels, TTx and cervicocentral LND is recommended. If the basal calcitonin level is elevated, LND should include the cervicolateral compartment.

Adolescent↗
PubMed2004

Multiple endocrine neoplasia 2B syndrome due to codon 918 mutation: clinical manifestation and course in early and late onset disease.

More than 50% of patients with typical MEN-2B have a de novo M918T germline mutation of the RET protooncogene. However, even in typical MEN-2B, extrathyroidal manifestations of MEN-2B can be found to be differently expressed. We analyzed the clinical manifestation and course in 21 patients harboring a de novo RET M918T mutation. Mean age at MEN-2B diagnosis was 14.2 years (range: 1-31 years). All patients had medullary thyroid carcinoma (MTC). At the time of syndrome diagnosis, oral manifestations (bumpy lips, ganglioneuroma), ocular manifestations (corneal fibers, conjunctivitis sicca), intestinal dysfunctions, musculoskeletal manifestations, and pheochromocytoma were found in 86%, 90%, 74%, 79%, and 19% of the patients, respectively. At the time of follow-up examination, the symptoms were found at higher frequency. Severe intestinal manifestation was predominantly found in patients with prepubertal onset (< or = 12 years) of MTC (n = 4/10) compared with patients with late onset (> 12 years) of MTC (n = 0/11) (40% versus 0%; p = 0.019). Although biochemical cure was found only in four patients with early onset of MTC, the long-term prognosis for patients with early onset of MTC was poorer than for patients presenting with late onset of MTC (p = 0.005). During mean follow-up of 55.8 months (range: 3-161 months), seven patients (33%) died from MTC. In conclusion, whereas most typical MEN-2B symptoms were found to be age-related, severe intestinal manifestation was found to be predominantly expressed in patients with early onset of MTC. Furthermore, in patients with early onset of MTC who could not be biochemically cured, the long-term prognosis was found to be worse than that of non-cured patients with late onset of MTC, suggesting an additional pathological process in the younger subgroup reinforcing the very high transforming in vitro activity of the M918T RET mutation.

Adolescent↗
PubMed2004

Timing and extent of surgery in patients with familial medullary thyroid carcinoma/multiple endocrine neoplasia 2A-related RET mutations not affecting codon 634.

In hereditary medullary thyroid carcinoma (MTC), recommendations regarding timing and extent of surgery are mainly based on the data of patients with the codon 634 RET mutation, which is the most often affected codon. Little is known about whether these recommendations may also be applied to patients with less common RET mutations. We ascertained the data from 140 patients with FMTC/MEN2A-related RET mutation not affecting codon 634 who have been treated at three specialized centers. The several RET mutations found affected codons 611 (n = 17), 618 (n = 22), 620 (n = 17), 768 (n = 9), 790 (n = 24), 791 (n = 21), 804 (n = 23), and 891 (n = 7). For each codon, the age of the youngest patient with MTC only (41, 7, 18, 29, 13, 47, 20, and 15 years, respectively), MTC with lymph node metastases (46, 24, 21, 34, 46, 47, 50, and 76 years, respectively), and MTC with distant metastases (52, 69, 43, 68, 57, - , - , and 75 years, respectively) was determined. All patients with lymph node metastases had elevated basal calcitonin levels. Based on these data, a more individual recommendation regarding timing and extent of surgery can be given. Because neither gender nor the type of nucleotide substitution for a specific codon appeared to have a significant influence on the age of onset, this recommendation should be based on the affected codon, the age of the patient, and the calcitonin level. Recurrent laryngeal nerve palsy (n = 6) and hypoparathyroidism (n = 3) were rather rare and were found only in patients older than 30 and 43 years, respectively, giving evidence that surgery in young patients can be performed safely.

Adolescent↗
PubMed2004

Gene expression of parathyroid tumors: molecular subclassification and identification of the potential malignant phenotype.

Parathyroid tumors are heterogeneous, and diagnosis is often difficult using histologic and clinical features. We have undertaken expression profiling of 53 hereditary and sporadic parathyroid tumors to better define the molecular genetics of parathyroid tumors. A class discovery approach identified three distinct groups: (1) predominantly hyperplasia cluster, (2) HRPT2/carcinoma cluster consisting of sporadic carcinomas and benign and malignant tumors from Hyperparathyroidism-Jaw Tumor Syndrome patients, and (3) adenoma cluster consisting mainly of primary adenoma and MEN 1 tumors. Gene sets able to distinguish between the groups were identified and may serve as diagnostic biomarkers. We demonstrated, by both gene and protein expression, that Histone 1 Family 2, amyloid beta precursor protein, and E-cadherin are useful markers for parathyroid carcinoma and suggest that the presence of a HRPT2 mutation, whether germ-line or somatic, strongly influences the expression pattern of these 3 genes. Cluster 2, characterized by HRPT2 mutations, was the most striking, suggesting that parathyroid tumors with somatic HRPT2 mutation or tumors developing on a background of germ-line HRPT2 mutation follow pathways distinct from those involved in mutant MEN 1-related parathyroid tumors. Furthermore, our findings likely preclude an adenoma to carcinoma progression model for parathyroid tumorigenesis outside of the presence of either a germ-line or somatic HRPT2 mutation. These findings provide insights into the molecular pathways involved in parathyroid tumorigenesis and will contribute to a better understanding, diagnosis, and treatment of parathyroid tumors.

Gene Expression Profiling↗
PubMed2004

Papillary and follicular thyroid carcinomas show distinctly different microarray expression profiles and can be distinguished by a minimum of five genes.

PURPOSE: We have previously conducted independent microarray expression analyses of the two most common types of nonmedullary thyroid carcinoma, namely papillary thyroid carcinoma (PTC) and follicular thyroid carcinoma (FTC). In this study, we sought to combine our data sets to shed light on the similarities and differences between these tumor types. MATERIALS AND METHODS: Microarray data from six PTCs, nine FTCs, and 13 normal thyroid samples were normalized to remove interlaboratory variability and then analyzed by unsupervised clustering, t test, and by comparison of absolute and change calls. Expression changes in four genes not previously implicated in thyroid carcinogenesis were verified by reverse transcriptase polymerase chain reaction on these same samples, together with eight additional FTC tumors. RESULTS: PTCs showed two distinct groups of genes that were either over- or underexpressed compared with normal thyroid, whereas the predominant changes in FTCs were of decreased expression. Five genes could collectively distinguish the two tumor types. PTCs showed overexpression of CITED1, claudin-10 (CLDN10), and insulin-like growth factor binding protein 6 (IGFBP6) but showed no change in expression of caveolin-1 (CAV1) or -2 (CAV2); conversely, FTCs did not express CLDN10 and had decreased expression of IGFBP6 and/or CAV1 and CAV2. CONCLUSION: PTC and FTC show distinctive microarray expression profiles, suggesting that either they have different molecular origins or they diverge distinctly from a common origin. Furthermore, if verified in a larger series of tumors, these genes could, in combination with known tumor-specific chromosome translocations, form the basis of a valuable diagnostic tool.

Adenocarcinoma, Follicular↗
PubMed2004

Repeat adrenocortical-sparing adrenalectomy for recurrent hereditary pheochromocytoma.

PURPOSE: Many endocrine surgeons advocate subtotal adrenalectomy for patients with bilateral hereditary pheochromocytoma despite the risk of recurrence. However, as the effectiveness of this procedure for locally recurrent pheochromocytoma is not well known, we investigated two patients who underwent this operation. METHODS: We performed repeat subtotal adrenalectomy for recurrent hereditary pheochromocytoma in two patients who had undergone primary subtotal adrenalectomy. RESULTS: Patient 1 was a 23-year-old woman with multiple endocrine neoplasia type 2A, in whom about 25% of the right adrenal gland was left in situ. Patient 2 was a 22-year-old man with von-Hippel-Lindau syndrome, in whom about 25% of both normal adrenal glands was left in situ. No steroid replacement was required postoperatively, and adrenocorticotropic hormone stimulation revealed sufficient adrenocortical function in both patients. No sign of recurrent pheochromocytoma has been found in 96 months and 11 months of follow-up, respectively. CONCLUSION: Recurrent hereditary benign pheochromocytoma after subtotal adrenalectomy may be treated successfully by repeated subtotal adrenalectomy. However, the risk of recurrence and malignancy must be weighed carefully against the risk of lifelong steroid replacement and potential Addisonian crisis. Thus, repeated subtotal adrenalectomy should be considered for selective patients who want to avoid steroid replacement.

Adrenal Gland Neoplasms↗
PubMed2004

Risk factors of paralysis and functional outcome after recurrent laryngeal nerve monitoring in thyroid surgery.

BACKGROUND: Recurrent laryngeal nerve monitoring (RLNM) has been suspected to reduce postoperative RLN paralysis (RLNP). However, functional outcome of RLNM in comparison with no nerve identification and visual nerve identification only has not been analyzed. METHODS: Analysis of 16,448 consecutive multi-institutional operations resulted in 29,998 nerves at risk. Three groups of different RLN treatment were compared: group 1, no RLN identification; group 2, visual RLN identification; and group 3, visual RLN identification and electromyographic monitoring. RLNM was performed with a bipolar needle electrode that was placed through the cricothyroid ligament into the vocal muscle. RESULTS: Risk factors for permanent RLNP were recurrent benign and malignant goiter (odds ratios, [ORs]), 4.7, and 6.7, respectively), primary surgery in thyroid malignancy (OR, 2.0), lobectomy (OR, 1.8), no nerve identification (OR, 1.4), low or medium volume hospital (OR, 1.3), and low volume surgeons (OR, 1.2). CONCLUSIONS: Based on these data, visual nerve identification was identified to be the gold standard of RLN treatment in thyroid surgery. RLNM is a promising tool for nerve identification and protection in extended thyroid resection procedures. However, because of the overall low frequency of RLNP, no statistical difference compared with visual nerve identification only was reached in the setting of this study.

Adolescent↗
PubMed2004

Expression of CD97 and CD55 in human medullary thyroid carcinomas.

The heterodimeric CD97 protein is a member of the EGF-TM7 family of class II seven-transmembrane (7TM) receptors of 75-90 kDa and structurally related to the secretin receptor family. CD97 is expressed on leucocytes, lymphocytes and in cells of the hematopoietic system. The precise role for CD97 is still unknown. The ubiquitously expressed CD55 (also known as decay accelerating factor, DAF) protects host cells from complement attack. In addition, CD55 is a bacterial/viral receptor and was identified as a ligand for CD97. Employing computer aided UV-laser microdissection CD97 and CD55 were investigated in C-cells of non-neoplastic thyroid specimens (n=3) and in medullary thyroid carcinomas (n=54) by multiplex RT-PCR. Frozen sections of all tissues were investigated by immunohistochemistry. All non-malignant thyroid specimens expressed CD97 mRNA weakly and were devoid of immunoreactive CD97 protein. Transcripts for CD97 were detected in all 54 MTC tissue specimens and CD97 gene activity directly correlated with the histopathological stage of the MTC. CD97 transcriptional activity was high in advanced stages of MTC such as pT3/4. pT1/2 tumors with exclusive intrathyroidal growth revealed weak CD97 expression. CD55 gene expression was significantly lower in normal C-cells than in tumor tissues and all MTC displayed strong and specific CD55 immunostaining. We did not observe a correlation between the expression of CD55 mRNA or protein, respectively, and pTNM classification. In summary, in the present study we have identified CD97 as a novel marker expressed in dedifferentiated neoplastic human thyroid C-cells. CD97 and CD55 may facilitate adhesion of C-cell carcinoma to surrounding surfaces which would result in rapid tumor cell spread.

Adolescent↗
PubMed2004

CD82, and CD63 in thyroid cancer.

CD82 (KAI1) and CD63 (ME491) are highly glycosylated proteins which belong to the transmembrane 4 superfamily (TM4SF). CD82 has been implicated as a possible prostate cancer metastasis suppressor gene, whereas CD63 is involved in the progression of human melanoma cancer. Down-regulation of both CD82 and CD63 expression has been associated with the metastatic potential of several solid tumors. Currently, information is lacking on the role of CD82 and CD63 during thyroid carcinogenesis. The aim of this study was to determine whether the expression of CD82 and CD63 is a useful prognostic indicator in patients with thyroid carcinoma. The expression of CD82 and CD63 was analysed by reverse transcriptase-PCR (RT-PCR) and immunohistochemistry in benign goiter (n=12) and 75 primary thyroid carcinoma tissue specimens (PTC: 33, FTC: 24, UTC: 18) out of which 36 were non-metastasized primary tumors and 39 were metastasized tumors (regional lymph node and/or distant metastases). All of the benign goiter tissues showed CD82 expression. By contrast, a significant decrease in CD82 mRNA and protein levels was detected in carcinoma tissues as compared to benign goiter tissues (p<0.001). A similar down-regulation was observed in metastasized tumor tissues when compared with non-metastasized tumors (all p<0.05). CD82 expression was correlated with pTNM status of differentiated and undifferentiated thyroid tumor and the pathologic stage of differentiated thyroid tumor. In contrast to CD82, CD63 mRNA and protein expression was unchanged in all thyroid carcinomas. Benign goiter tissues showed weak expression of CD63. There were no significant correlation between CD63 mRNA/protein expression and any clinical/pathological parameters. Our results support the hypothesis that down-regulation of CD82 expression may reflect an increased in vivo metastatic potential of thyroid cancer cells. CD82 may serve as a prognostic marker of metastasis in thyroid cancer. Constitutive expression of CD63 may indicate that this factor does not play a direct role in thyroid carcinogenesis.

Adolescent↗
PubMed2003

Frequent RASSF1A promoter hypermethylation and K-ras mutations in pancreatic carcinoma.

Recently, we have characterized the Ras association domain family 1A gene (RASSF1A) at the segment 3p21.3, which is frequently lost in variety of human cancers and epigenetically inactivated in many types of primary tumors, such as lung, breast, kidney, prostate and thyroid carcinomas. Here, we investigated the methylation status of the RASSF1A CpG island promoter in the pathogenesis of pancreatic cancer. RASSF1A hypermethylation was detected in 29 out of 45 (64%) primary adenocarcinomas, in 10 out of 12 (83%) endocrine tumors and in eight out of 18 (44%) pancreatitis samples. In seven out of eight pancreas cancer cell lines, RASSF1A was silenced and was retranscribed after treatment with 5-aza-2'-deoxycytidine. Additionally, we analysed the aberrant methylation frequency of cell cycle inhibitor p16(INK4a) and K-ras gene mutations in the pancreatic samples. p16 inactivation was detected in 43% of adenocarcinomas, in 17% of neuroendocrine tumors, in 18% of pancreatitis and in 63% of pancreas cancer cell lines. K-ras mutations were detected in 16 out of 45 (36%) primary adenocarcinomas. Pancreatic adenocarcinomas with K-ras mutation have significantly less RASSF1A methylation and vice versa (P=0.001, chi(2) test). In conclusion, our data indicate that inactivation of the RASSF1A gene is a frequent event in pancreatic cancer and suggest an inverse correlation between RASSF1A silencing and K-ras activation.

Codon↗
PubMed2003

Caveolin-1 and caveolin-2,together with three bone morphogenetic protein-related genes, may encode novel tumor suppressors down-regulated in sporadic follicular thyroid carcinogenesis.

Thyroid cancer is common, occurring in 1% of the general population. The relative frequencies of two of the most common subtypes of thyroid carcinoma, follicular (FTC) and papillary (PTC), vary depending on the regional prevalence of iodine deficiency. Although PTC has been more extensively studied, the etiology of sporadic FTC is poorly understood. To further elucidate this, we conducted microarray expression comparison of FTC tumors and normal thyroid tissue. Three commonly down-regulated genes, caveolin-1, caveolin-2, and GDF10/BMP3b, were chosen for further study on the basis of their localization to two chromosomal regions, 7q31.1 and 10q11.1, that commonly show loss of heterozygosity in FTC. Two additional genes, glypican-3 and a novel chordin-like gene, were also analyzed in view of their involvement in bone morphogenetic protein signaling and possible interaction with GDF10. Each of these five genes was down-regulated in >or=15 of 19 FTC tumors (79%) by semiquantitative reverse transcription-PCR. Caveolin-1 showed preferential down-regulation of its beta-isoform at both the mRNA and protein level, suggesting a distinct function for this isoform. Caveolin-1 is of particular functional interest because it has been shown to interact with PTEN, the tumor suppressor gene mutated in Cowden syndrome, an inherited multiple hamartoma syndrome that includes predisposition to FTC. Immunohistochemical analysis of 141 thyroid tumors of various histological types showed significantly fewer caveolin-1-positive tumors in FTCs, including insular type tumors, and Hurthle cell carcinomas in comparison with normal thyroid. PTC and anaplastic thyroid carcinomas did not show significant down-regulation, and thus, caveolin-1 may become a useful molecular marker to differentiate the various histologies of thyroid malignancies.

Adenocarcinoma, Follicular↗
PubMed2003

Peroxisome proliferator-activated receptor gamma is frequently downregulated in a diversity of sporadic nonmedullary thyroid carcinomas.

Peroxisome proliferator-activated receptor gamma (PPARgamma) has previously been implicated in the pathogenesis of follicular thyroid carcinoma (FTC), where a translocation with PAX8 has been reported in some 50% of tumors in three small series. The resultant fusion protein inhibits normal PPARgamma function by a dominant-negative mechanism. In a series of 19 FTCs, we identified this translocation in only two tumors (10.5%). However, microarray analysis and semiquantitative RT-PCR demonstrated greatly reduced PPARgamma expression in 13 of 17 (76%) nontranslocation tumors. Immunohistochemical analysis of 142 thyroid tumors showed a statistically significant reduction in PPARgamma immunoreactive protein, not only in FTCs but also in papillary thyroid carcinomas and Hurthle cell carcinomas. This suggests that while the overall frequency of the PAX8-PPARgamma translocation in FTCs may be lower than previously thought, functional downregulation of PPARgamma is a key event in multiple types of thyroid neoplasia and is a possible target for therapeutic intervention.

Carcinoma↗
PubMed2003

Functional results after endoscopic subtotal cortical-sparing adrenalectomy.

PURPOSE: We examined the required amount of residual adrenal tissue and whether an intact adrenal vein are necessary to achieve sufficient function after endoscopic subtotal adrenalectomy. METHOD: Endoscopic subtotal adrenalectomy was performed in 14 patients. Two patients underwent unilateral subtotal and contralateral total adrenalectomy and another two patients underwent unilateral subtotal adrenalectomy after contralateral total adrenalectomy several years earlier. We analyzed the postoperative serum levels of cortisol and adrenocorticotropic hormone (ACTH). Patients with bilateral tumors underwent an ACTH test. RESULTS: We had to cut the main adrenal vein in ten patients, and less than one third of the adrenal gland was left in situ in four patients. Subtotal adrenalectomy was performed unilaterally in two patients with bilateral tumors. One third of the adrenal gland was preserved in these patients, and also in the two patients with unilateral subtotal adrenalectomy after previous contralateral total adrenalectomy. The postoperative ACTH test confirmed satisfactory adrenocortical function. During the follow-up period of about 24 months no recurrent tumors have been found. CONCLUSION: Subtotal cortical-sparing adrenalectomy can be successfully performed laparoscopically. The venous drainage of the main adrenal vein does not seem to be crucial for sufficient adrenocortical function. We estimate that leaving about one third of the entire adrenal gland as remnant adrenal tissue will result in sufficient function.

Adrenal Cortex↗
PubMed2003

Critical size of residual adrenal tissue and recovery from impaired early postoperative adrenocortical function after subtotal bilateral adrenalectomy.

BACKGROUND: Subtotal bilateral adrenalectomy may preserve adrenocortical function. Little is known about the early postoperative function of the adrenal remnant. METHOD: In 10 patients with bilateral adrenal tumors (pheochromocytomas, adrenocortical nodular hyperplasia, and adrenal metastases), plasma adrenocorticotropic hormone (ACTH), serum cortisol, and maximal cortisol liberation were examined with an ACTH test after subtotal bilateral adrenalectomy, which left 15% to 30% of adrenal tissue in situ. RESULTS: In the early postoperative period, all patients had normal basal serum cortisol levels (mean, 415+/-208 nmol/L; normal morning range, 138-690 nmol/L) but pathologically increased plasma ACTH levels (mean, 55+/-42 pmol/mL; normal, <10.1 pmol/L). In 6 patients, a pathologic ACTH test result was observed. During follow-up (mean, 11.3+/-7.6 months), all patients were found to have a normal ACTH test result. None of the patients required steroid supplementation. However, in patients with both familial pheochromocytoma and impaired adrenocortical function during the early postoperative period, the maximal increase of serum cortisol after ACTH stimulation was significantly reduced (mean, 301+/-86.8 nmol/L) compared with control subjects (mean, 490+/-132.6 nmol/L; P=.019). CONCLUSION: After subtotal bilateral adrenalectomy left 15% to 30% of adrenal tissue in situ, functional recovery could be observed in all patients. However, subclinical impairment of the adrenocortical function with questionable clinical significance has to be considered in some of the patients. Especially during the early postoperative period, careful observation of the patients without exogenous steroid administration is required.

Adrenal Cortex Function Tests↗
PubMed2002

Primary hyperparathyroidism, C-cell hyperplasia and papillary thyroid carcinoma in a patient with RET germline polymorphism S836S.

BACKGROUND: In most examined populations the RET germline polymorphism S836S is found in about 3.6% of the normal population but in about 9% of patients suffering from sporadic C-cell hyperplasia or medullary thyroid carcinoma. The polymorphism S836S is thought to be involved in the development of sporadic medullary thyroid carcinoma. CASE PRESENTATION: We report a 48-year-old woman suffering from primary hyperparathyroidism (parathormone 121-166 pg/ml, normal <72), bilateral diffuse and nodular C-cell hyperplasia (calcitonin after pentagastrin administration 156 pg/ml, normal <4.6), and papillary thyroid carcinoma. Two commercial analyses of RET did not reveal any germline mutation within the known hot spots. However, sequencing revealed the presence of the RET polymorphism S836S. Following total thyroidectomy and removal of two hyperplastic parathyroid glands parathormone decreased to 51 pg/ml and calcitonin was no longer detected. CONCLUSIONS: The pathogenetic importance of the RET polymorphism S836S is still obscure. However, according to the published overrepresentation of the RET polymorphism S836S in patients suffering from apparent sporadic medullary thyroid carcinoma, it is conceivable that it also plays a role in multiglandular endocrine disease.

Carcinoma, Papillary↗