Shaken baby syndrome: intending to harm or attempting to help?

PURPOSE: To describe the role of ophthalmologists in shaken baby syndrome evaluation. METHODS: Case report. RESULTS: A 3.5-month-old girl was admitted to the Pediatrics Clinic with lethargy. The mother, who brought in the baby, claimed that the baby had fallen from her cradle 6 hours ago. Clinical examination showed signs of head injury. Ophthalmologic examination was requested and revealed extensive retinal hemorrhages bilaterally covering the whole fundus, and retrohyaloid hematoma in the right eye. Computerized tomography neuroimaging documented large subdural hematomas exerting force on the brain parenchyma. The sum of the results of the clinical and neuroimaging examination-retinal hemorrhages and subdural hematomas-was indicative of violent shaking of the baby. Coronal evaluation was unable to determine whether the baby was abused by her parents or whether she was accidentally hurt. CONCLUSIONS: Ophthalmologic examination is necessary to document shaken baby syndrome since it reveals the retinal hemorrhages which together with the neuroimaging findings are almost always present in such cases. However, even when all the signs of shaken baby syndrome are present, it is difficult and sometimes destructive for a parent to be falsely accused of abusing his or her own child.

Dermatofibrosarcoma protuberans occuring in a child.

Dermatofibrosarcoma protuberans (DFSP) usually occurs in adults, however it can also occur in infancy and childhood. Diagnosis of DFSP in children is quite difficult given the rarity of the tumor and its variegated appearance. The behavior of this neoplasm is of borderline or intermediate malignancy with a high rate of recurrence but limited metastatic potential. We present the case of an eleven-year old boy who presented with a slightly raised, not tender lesion on his right shoulder. It had appeared two years before as a red-brown plaque and since then it had gradually grown to a nodule. An excisional biopsy was performed, and the diagnosis of DFSP was made based on the histological and immunohistochemical findings.

Genetic models of human cancer as a multistep process. Paradigm models of colorectal cancer, breast cancer, and chronic myelogenous and acute lymphoblastic leukaemia.

Tumour formations arise as a consequence of alterations in the control of cell proliferation as well as with disorders in interactions between cells and their environment that result in invasion and metastasis. Recent advances in understanding the genetic basis of malignant diseases have been dominated by research in colorectal cancer. Genetic alterations of several proto-oncogenes and tumor-suppressor genes (e.g. APC/MCC, RAS, DCC, p53 mutations and/or allelic losses, hyperexpression of c-MYC and RB genes), as well as other genomic alterations, appear at characteristic stages of tumor development and are observed in most neoplasms. Generally, the normal cell has multiple independent mechanisms that regulate its growth and differentiation potential, and several separate events would, therefore, be needed to override these control mechanisms, as well as induce the other aspects of the transformed phenotype, like metastasis. These signals may be either positive or negative, and the acquisition of tumorigenicity results from genetic changes that affect these control points following a multistep mode. Statistics of the frequency of cancer incidence with age in humans indicate that for the genesis of e.g. lung carcinoma, five or six steps are required. Other types of cancers, such as leukemias and sarcomas, probably require quite a different number of rate-limiting changes. One of the best characterized tumours to provide a genetic model is colorectal tumorigenesis. Mutations implicated in breast cancer tumorigenicity are also studied and used as a genetic model in the literature worldwide. Finally, activation of c-abl in chronic myelogenous leukaemia (CML) and acute lymphoblastic leukaemia could also be presented as an example, which provides probably the strongest evidence for the role of proto-oncogenes in human malignancy process.

Cell cycle proteins in laryngeal cancer: role in proliferation and prognosis.

A study of laryngeal carcinomas was performed in order to analyze (a) the expression of p53/p21, cyclin D1/cyclin E, p21/p27 (b) the relation of normal and abnormal protein expression, with the proliferation status, as determined by the expression of Ki67 and PCNA and (c) the correlation of our findings with prognosis. We performed a retrospective analysis of 57 cases of squamous cell carcinomas of the larynx. We applied monoclonal antibodies against p53, p21, p27, cyclin D1, cyclin E, Ki67 and PCNA, using streptavidin-biotin method. Analysis of the p53/p21 proteins, revealed abnormalities in 25/37 cases (67.57%), while 12/37 (32.43%) cases displayed normal phenotype (p53-/p21-). Analysis of cyclins revealed overexpression in 17/48 cases (35.42), while the majority 31/48(64.58%) displayed normal phenotype (cyclin D1-/cyclin E-). Concerning CDKIs expression, the majority 30/50(60%) presented high levels of both inhibitors (p21+/p27+). Cases with simultaneous overexpression of CDKIs demonstrated significantly higher levels of Ki67 protein (p = 0.05). Analysis of p53/p21, cyclin D/cyclin E, p21/p27 patterns showed no association between the presence of one or two alterations and prognosis. In conclusion, we demonstrated that p53 tumor suppressor pathway is frequently disrupted in laryngeal cancer. Furthermore, levels of CDKIs, although they act as cell cycle activity blockers, are not reliable markers for the estimation of laryngeal neoplastic cells growth fraction.

Giant simple renal cyst complicated with hypertension.

Solitary renal cysts are a common and usually asymptomatic occurrence in older patients. They may be associated with hypertension or abdominal disturbances, as they can be responsible for compression of surrounding tissues and distortion of renal vessels. This report presents an interesting case of a hypertensive patient with a solitary renal cyst of a marked size. Owing to the high risk of performing a surgical procedure in such a patient, a distinct therapeutic solution was opted for. Successful management of this case was achieved by a combination of percutaneous fluid aspiration and injection of alcohol and Vibramycin inside the cystic cavity. Percutaneous fluid evacuation combined with the administration of a sclerosing agent is suggested as a safe and effective alternative for cyst decompression and blood pressure normalisation.

Glycoprotein CD44 expression in benign, premalignant and malignant epithelial lesions of the larynx: an immunohistochemical study including correlation with Rb, p53, Ki-67 and PCNA.

CD44 is an integral membrane glycoprotein that has diverse functions in cell-cell and cell-substrate interactions. It has been suggested that it may be a determinant of metastatic and invasive behavior in carcinomas. The immunohistochemical expression of CD44 was examined in a series of 34 squamous cell carcinomas, 13 in situ carcinomas, 35 cases with various degrees of epithelial dysplasia, 10 papillomas and 17 cases of keratosis. We used the monoclonal mouse anti-human phagocytic glycoprotein-1 CD44 (clone DF 1485), on formalin-fixed, paraffin-embedded tissue. CD44 expression was correlated with the expression of Rb and p53 proteins, with the proliferative indices Ki-67 and PCNA as well as with conventional clinicopathological data. The mean value of CD44 expression was 78.84 in squamous cell carcinomas, 78.04 in situ carcinomas, 54.93 in dysplasia, 26.8 in papillomas and 24.97 in keratosis. There was no significant difference of CD44 expression between in situ and invasive carcinomas. However, a strong difference of reaction between carcinomas and the other cases was observed. CD44 expression was statistically higher in dysplastic lesions than the cases of keratosis (p < 0.0001) and papillomas (p = 0.01). In the group of invasive carcinomas, CD44 expression was statistically correlated with pRb (p = 0.011), while in preinvasive lesions it was correlated with PCNA (p = 0.016). The relationship with the degree of dysplasia or grade of carcinoma and p53 protein expression was insignificant. These observations suggest that CD44 expression may be involved in the multiple mechanism of the development and progression of laryngeal lesions and may help to predict the risk of transformation of the benign or precancerous lesions to cancer.

Expression of the extracellular matrix protein tenascin in laryngeal epithelial lesions: correlation with fibronectin, CD44, cathepsin D and proliferation indices.

Tenascin (TN) is an extracellular matrix glycoprotein expressed in areas of epithelial-mesenchymal interactions during embryogenesis and in neoplasia. We studied the expression of TN in a series of 35 squamous cell invasive carcinomas of the larynx, 13 in situ carcinomas, 41 cases of dysplasia, 10 papillomas and 18 cases of keratosis using the monoclonal antibody TN2 on paraffin-embedded tissue. TN expression was correlated with the expression of fibronectin, CD44 and cathepsin D (CD) proteins, with the proliferation indices Ki-67 and proliferating cell nuclear antigen (PCNA) as well as with conventional clinicopathological variables. Malignant tumours showed a significantly greater stromal TN staining than benign lesions. In invasive carcinomas, the immunoreactivity was statistically higher than that in situ (P=0.01), dysplastic lesions (P<0.0001), papillomas (P=0.004) and keratosis (P<0.0001). A statistically significant difference of TN expression between in situ and dysplastic lesions was observed (P=0.001). In invasive lesions, TN expression was statistically correlated with CD44 expression (P=0.02) and a trend for correlation with CD of tumour cells and fibronectin expression was found (P=0.06 and P=0.09, respectively). The relationship of TN expression with the histological grade and the proliferative activity was insignificant. In conclusion, stromal TN expression may be involved in the complex mechanism of development of laryngeal lesions and may help to predict the risk of progression of pre-cancerous lesions to cancer.

Altered patterns of retinoblastoma gene product expression in benign, premalignant and malignant epithelium of the larynx: an immunohistochemical study including correlation with p53, bcl-2 and proliferating indices.

In order to study the altered Rb, bcl-2 and p53 proteins expression during laryngeal carcinogenesis and to elucidate the role of these molecules in the development and progression of the lesions, we have examined the immunohistochemical expression of these markers in a series of 41 squamous cell carcinomas, 14 cases of in situ carcinoma, 47 with epithelial dysplasia, 11 papillomas and 20 cases of keratosis. Rb protein was expressed in 69.7% (> 5% positive neoplastic cells) of squamous cell carcinomas and p53 in 40% (> 5% positive cells). There was a strong statistically significant difference for Rb, Ki-67 and PCNA immunostaining between malignant, premalignant and benign lesions, increasing from keratosis, papillomas, dysplasia to carcinoma in situ or infiltrating squamous Ca. Rb protein expression was also strongly correlated with p53, Ki-67 and PCNA, while p53 protein was strongly correlated with Ki-67 (p = 0023) and PCNA (p = 0.0031) indices, in all lesions. In conclusion Rb and p53 altered proteins expression seems to play an active role in laryngeal carcinogenesis, probably from the early phase, and is correlated with proliferative activity. Also, Rb protein expression is correlated with the progression of the lesion and could be considered as indication of poor prognosis in laryngeal lesions.

Immunohistochemical expression of cathepsin D in laryngeal epithelial lesions: correlation with CD44 expression, p53 and Rb status and proliferation associated indices.

Clinical studies in several tumour types have shown a strong correlation between cathepsin D expression and tumour progression. Immunohistochemical staining for cathepsin D (clone D13A) was performed in paraffin embedded-tissues from 39 invasive squamous cell carcinomas, 13 in situ carcinomas, 35 cases of dysplasia, 10 papillomas and 17 cases of keratosis. The association between cathepsin D expression and CD44, p53, Rb proteins and proliferation indices (Ki-67, PCNA) was assessed by univariate analysis. Cathepsin D was highly positive in the groups of carcinomas compared to other lesions (p < 0.0001). A statistically significant correlation of cathepsin D expression with CD44 expression was observed in invasive cancers (p = 0.037). The relationship of cathepsin D immunoreactivity with p53, Rb and proliferation indices was insignificant. The results show that cathepsin D is expressed in a higher proportion of cancerous lesions of the larynx than in non cancerous or premalignant lesions, a fact which suggests that cathepsin D may be involved in laryngeal tumour cell growth process.

Immunohistochemical expression of metallothionein in benign premalignant and malignant epithelium of the larynx: correlation with p53 and proliferative cell nuclear antigen.

In this study we evaluated the immunohistochemical expression of metallothionein (MT) in 44 squamous cell carcinomas, 14 cases of in situ carcinoma, 47 with epithelial dysplasia, 11 papillomas and 21 cases of keratosis. The MT expression was studied in correlation with p53 protein expression and the proliferative cell nuclear antigen (PCNA). The monoclonal antibodies E9 (anti-MT), DO-7 (which reacts with a denaturation-resistant epitope in wild-type and mutant p53) and PC10 (anti-PCNA) on formalin-fixed, paraffin-embedded tissue were used employing the immunoperoxidase (ABC) method. The immunohistochemical localization of MT has shown its rather ubiquitous presence in the cytoplasm and nucleus of both benign and malignant epithelial cells. In most cases the adjacent "normal" epithelium showed low positivity in the basal portion. The mean value of metallothionein expression was 35.73 in squamous cell carcinomas, 32.21 in in situ carcinomas, 11.86 in dysplastic epithelium, 5.10 in papillomas and 3.5 in keratosis. In carcinomas, low MT expression (< 10% of neoplastic cells) was observed in 20.5% of the cases, moderate (10%-50% of neoplastic cells) in 54.5% and extensive expression (> 50% of neoplastic cells) in 25% of the cases. We did not find any statistically significant difference of MT expression between in situ and infiltrating carcinomas, while we did observe a significant difference between carcinomas and the other groups. There was a statistically significant difference in the PCNA values in both benign and malignant lesions, while no statistically significant difference was observed in p53 protein expression in the above groups. A positive correlation between MT expression and the PCNA value (p < 0.0001) in the benign and malignant groups was detected. The PCNA value was also correlated with the p53 protein expression (p = 0.001). No correlation was found between MT and p53 protein expression. In conclusion, these results suggest that the MT expression may play a role in the development of malignant disease of the larynx, from the early phase of laryngeal carcinogenesis, independently from the p53 expression. It is also possible to contribute to tumour cell growth, as determined by the PCNA score.

Expression patterns of cyclins D1, E in laryngeal epithelial lesions: correlation with other cell cycle regulators (p53, pRb, Ki-67 and PCNA) and clinicopathological features.

The expression of cell-cycle progression molecules cyclin D1 and cyclin E were immunohistochemically examined in a series of 64 squamous cell invasive carcinomas of the larynx, 10 in situ carcinomas, 34 cases of dysplasia, 11 papillomas and 23 cases of keratosis. The results of their expression were compared with two cell-cycle implicated tumor suppressor proteins p53 and pRb as well as with two proliferation associated indices PCNA and Ki-67 in an attempt to elucidate their potential role in the pathogenesis and progression of these lesions. Nuclear staining for cyclin D1 and E (>5% positive cells) was observed in 19% and 39.7% of the laryngeal carcinomas, respectively. Significantly elevated levels of cyclin D1 and E in invasive laryngeal carcinomas compared with in situ carcinomas were revealed (p=0.045 and p=0.0003, respectively). High levels of cyclin D1 and E expression were correlated with increased Ki-67 score (p=0.037 and 0.017 respectively). A significant positive correlation between cyclin D1 and E was also detected in carcinomas (p=0.018). Decreased levels of cyclins D1 and E in the group of in situ carcinomas compared with those of dysplastic cases and papillomas were also observed. In the dysplastic lesions cyclin D1 expression was correlated with pRb expression (p=0.02). In the cases of keratosis cyclins D1 and E expression were correlated with pRb (p=0.002 and p=0.036, respectively), while cyclin D1 was associated with PCNA (p=0.008) and Ki-67 score (p=0.009). The prognostic significance of cyclins D1, E in determining the risk of recurrence and overall survival with both univariate (long-rang test) and multivariate (Cox regression) methods of analysis showed no statistically significant differences. We conclude that the expression of cyclins D1 and E in squamous cell carcinomas of the larynx does not seem to have a prognostic significance. In addition, their expression may be involved in the development of laryngeal lesions, implicated in cell proliferation, with other cell cycle related proteins, probably by different molecular pathways.

Expression of cyclin-dependent kinases inhibitors p21(WAF1) and p27(KIP1) in benign, premalignant and malignant laryngeal lesions. correlation with cell cycle regulatory proteins.

BACKGROUND: Cell cycle progression and transition of cells from the first gap phase (G1) to the DNA replication phase (S) depend on a finely tuned balance between the levels of cyclins, cyclin-dependent kinases (CDKs) and cyclin-dependent kinase inhibitors (CDKIs). MATERIALS AND METHODS: We analyzed 57 squamous cell invasive carcinomas of the larynx, 10 in situ carcinomas, 56 cases of dysplasia, 11 papillomas and 26 keratosis. We investigated: a) the immunohistochemical expression of CDKIs, p21 and p27, b) any possible relation between normal and abnormal immunoprofiles of these proteins and p53 protein and proliferation status as determined by the expression of Ki67 and PCNA, and c) their presence in pre-malignant and malignant laryngeal lesions. RESULTS: Expression of p21 and p27 was observed in 58.9% and 89.5% of the laryngeal carcinomas, respectively. High levels of p21 were significantly correlated with increased cyclin D (p=0.001), cyclin E (p<0.001) and Ki67 (p<0.001), while increased expression levels of p27 were associated with p53 accumulation (p=0.02) and with increased proliferation status as expressed by Ki67 (p=0.05). CONCLUSION: Due to the increased expression levels of CDKIs in laryngeal carcinomas, we suggest the existence of a mechanism by which tumor cells tolerate the inhibitory effect of these proteins on cell cycle progression.

The role of ascorbic acid, selenium, and glutathione on benzo[a]pyrene-induced carcinogenesis in wistar rats.

PURPOSE: The carcinogenic action of polycyclic aromatic hydrocarbons (PAHs) can be inhibited by endogenous or exogenous compounds. This study was designed to elucidate the modifying action of 3 endogenous inhibitors- ascorbic acid (vit C) used alone, and selenium (Se) used in combination with glutathione (GSH). MATERIALS AND METHODS: Chemical carcinogenesis was induced by benzo[a]pyrene(BaP). A hundred wistar rats were divided into 3 groups: the first group (G I) consisted of 42 animals, representing the control group. The two experimental groups (G II and G III) consisted of 38 and 20 rats, respectively. All groups were injected with BaP(10.08 mg subcutaneously-s.c). The first experimental G II was given only vit C (520 mg in 2% sugar solution per os - p.o.). The second experimental G III was given Se (0.1 mg p.o.) with GSH (200 mg p.o.). Tumor incidence and mean survival time were determined. Histological examination of the developed and excised tumors took place following death. The carcinogenic potency (CP) and anticarcinogenic potency (AP) of the substances used were calculated. RESULTS: A statistically significant difference regarding the mean survival time in the two experimental groups (238.4-/+31 days and 344.9-/+48 days, respectively) compared to the control group (183.8-/+28 days) was found (p < 0.001). The CP of each of the 3 groups was 54.3, 41.2, and 28.9 units, respectively. The AP of vit C used alone was 13.1 units, representing a significant anticarcinogenic effect. The combination of Se + GSH showed an AP of 25.4 units, resulting in a significant prolongation of the mean survival time, which is considered a potent anticarcinogenic effect. Furthermore, a statistically significant difference was found also when the mean survival time of G III animals was compared with G II. CONCLUSION: Vit C on its own and Se in combination with GSH represent strong endogenous inhibitors that can inhibit/reduce the carcinogenic action of BaP-induced carcinogenesis in wistar rats. The combination therapy used offered better in vivo results.

Amplification and co-regulators of androgen receptor gene in prostate cancer.

Prostate cancer is the second most common malignancy among males after lung cancer. The growth of prostate cancer cells depends on the presence of androgens, a group of steroid hormones that include testosterone and its more active metabolite dihydrotestoste-rone. Most prostate cancers are androgen-dependent and respond to the antiandrogens or androgen-deprivation therapy. However, the progression to an androgen-independent stage occurs frequently. Possible mechanisms that could be involved in the development of hormone resistant prostate cancer causes including androgen receptor (AR) mutations, AR amplification/over expression, interaction between AR and other growth factors, and enhanced signaling in a ligand-independent manner are discussed.

Molecular profiling and genomic microarrays in prostate cancer.

In the present review article a global approach regarding the usefulness of genomic microarrays in prostate cancer management, is attempted. Cancer is a multistep process of mutations in key regulatory genes and epigenetic alterations that result in loss of balanced gene expression. A complete knowledge of the interaction between the genetic variability of the neoformation (tumor profiling) and the genetic variability of the host (inherited genome profiling), will be able to determine the better strategy against the cancer and the less toxicity for the patient. Alterations in the sequence of the hormone binding domain of the androgen receptor as well as mutations in some genes, determine radioresistance and resistance or sensitivity to some chemotherapeutic drugs. New therapies using monoclonal antibodies directed against specific extracellular binding domains of some receptors are based on molecular alterations observed in tumors.

E-cadherin adhesion molecule and syndecan-1 expression in various thyroid pathologies.

UNLABELLED: Cadherins and syndecans are transmembrane glycoproteins implicated in cell-cell and cell-matrix adhesion. Impairment of cadherin and syndecan mediated adhesion is likely to constitute one of the main factors leading to the reduced cell-cell and cell-matrix adhesion characteristics of tumor cells and play a pivotal role in the acquisition of invasive and metastatic proprieties by neoplastic epithelial cells. AIM: To elucidate the role and alterations of syndecan-1 expression in comparison with those of E-cadherin in normal and pathological thyroid glands (TG). METHODS: A total of 55 TG carcinomas, 40 TG adenomas, 40 cases of hyperplastic TG disorders and 20 cases of normal TG autopsy samples, were evaluated by immunohistochemistry. The staining intensity, and localization of syndecan-1 and E-cadherin in sequential sections were examined, and semi-quantified. RESULTS: Immunostaining of syndecan-1 and E-cadherin was strong in normal follicular TG epithelial cells, and located mainly in basolateral membrane. No significant change was seen in either molecule in hyperplastic TG disorders compared with TG adenomas. A significant reduction in expression of both syndecan-1 and E-cadherin was seen in well-differentiated TG carcinomas as compared with normal TG epithelium (p = 0.0001 and p = 0.032, respectively). Similarly, there was a significant reduction of both molecules expression in poorly differentiated and anaplastic TG carcinomas compared to well differentiated tumors (syndecan-1: p = 0.0037; and E-cadherin: p = 0.075). CONCLUSION: Decreased E-cadherin and syndecan-1 expression along with decreasing cellular differentiation may be involved in the complex mechanism of progression of TG pathology.

Thoracoabdominal wall tumour seeding after percutaneous radiofrequency ablation for recurrent colorectal liver metastatic lesion: a case report with a brief literature review.

Radiofrequency is a safe and effective minimally invasive procedure in the treatment of liver and other organs neoplastic lesions. Percutaneous access of neoplastic liver tissue is the most common access and electrodes are placed with imaging guidance into the tumour to be ablated. Complications during and after radiofrequency ablation (RFA) are of major or minor severity. Tumour dissemination related to the percutaneous access seems to be very unusual. Herein, we present a rare case of thoracoabdominal tumour wall dissemination after RFA of a recurrent hepatic colorectal metastasis previously removed by surgery. A 64-year-old man with a recurrent hepatic metastatic lesion was treated with internally cooled radiofrequency (RF) for ablation of a 3x3 cm in size tumour mass. Two sessions of RFA in one-month period were performed. Computed tomography (CT) of the upper abdomen and carcinoembryonic (CEA) antigen were used for estimation of the disease progression in the patient's follow-up. Ten months after RFA the patient presented abdominal pain and a mass appeared on the right thoracoabdominal area with simultaneous lung metastases. In conclusion, a large size, bulky and superficial mass on the liver parenchyma adjacent to the thoracoabdominal wall as well as multiple RFA sessions, seem to represent risk factors for tumour dissemination through the needle electrode used during the RFA procedure in hepatic metastases of colorectal cancer.

In breast carcinoma dysadherin expression is correlated with invasiveness but not with E-cadherin.

Reduction/loss of E-cadherin is associated with the development and progression of many epithelial tumours. Dysadherin, recently characterised by members of our research team, has an anti-cell-cell adhesion function and downregulates E-cadherin in a post-transcriptional manner. The aim of the present study was to study the role of dysadherin in breast cancer progression, in association with the E-cadherin expression and the histological type. We have selected ductal carcinoma, which is by far the most common type and lobular carcinoma, which has a distinctive microscopic appearance. Dysadherin and E-cadherin expression was examined immunohistochemically in 70 invasive ductal carcinomas, no special type (NST), and 30 invasive lobular carcinomas, with their adjacent in situ components. In ductal as well as in lobular carcinoma dysadherin was expressed only in the invasive and not in the in situ component, and this expression was independent of the E-cadherin expression. Specifically, all 10 (100%) Grade 1, 37 out of 45(82.2%) Grade 2 and six out of 15 (40%) Grade 3 invasive ductal carcinomas showed preserved E-cadherin expression, while 'positive dysadherin expression' was found in six out of 10 (60%) Grade 1, 34 out of 45(75.5%) Grade 2 and all 15 (100%) Grade 3 neoplasms. None of the 30 infiltrating lobular carcinomas showed preserved E-cadherin expression, while all the 30 infiltrating lobular carcinomas exhibited 'positive dysadherin expression'. Dysadherin may play an important role in breast cancer progression by promoting invasion and, particularly in lobular carcinomas, it might also be used as a marker of invasion.

Acute septic cholelithiasic cholecystitis and adenocarcinoma of the gallbladder; an interesting association.

BACKGROUND AND STUDY AIMS: Primary carcinoma of the gallbladder may present as acute lithiasic cholecystitis that leads to severe septic complications. The correlation between severe sepsis of the gallbladder and primary carcinoma is unclear. The goal of the present study is to examine the relation between severe septic complications of lithiasic cholecystitis and primary carcinoma of the gallbladder. PATIENTS AND METHODS: A group of 72 patients (22 males, 50 females, age range: 45-99, mean age: 68.6 years), with severe septic cholelithiasic cholecystitis was treated with emergency surgery after failure of conservative treatment, and patients found with primary carcinoma of the gallbladder were registered. The resectability and operability of the tumor were studied, as well as tumor staging and overall patient survival. RESULTS: During urgent surgery for severe septic lithiasic cholecystitis, 12 patients (12/72, 16.6%) were found with gallbladder carcinoma. Patients with septic acute lithiasic cholecystitis and carcinoma had a higher mean age compared to those without carcinoma (74.8 vs. 67.4 yrs). Eleven of 12 (91.6%) carcinomas were inoperable, despite resectability of 8 out of 12 (66.6%), and overall patient survival was limited to a few months after surgery. CONCLUSIONS: Severe septic complications in elderly patients with a long-standing history of gallbladder stones may co-exist with primary carcinoma of the gallbladder. The percentage of a gallbladder carcinoma detected in septic patients reaches up to 16.6%. Even if these patients have a poor general health, surgical intervention is a solution when they appear with severe septic clinical symptoms caused by gallstones or carcinoma, in order to avoid lethal sepsis. The possibility of a carcinoma hidden in the gallbladder must be in mind during surgery. Imaging studies before surgery may detect the carcinoma; in most cases carcinomas are inoperable, although colecystectomy may be performed during surgery.