A Clinical Study on Gallbladder Polyp.

There are different types of gallbladder polyps having variable morphology and nature. Symptoms are vague and mostly diagnosed incidentally on abdominal ultrasound. Risk factors are many. Indications of surgery are not clearly understood due to lack of clinical evidence. This study was carried out to analyze the management of gallbladder polyp in our settings and review of available evidence. Patients who underwent clip less mini laparoscopic cholecystectomy for gallbladder polyp were included. Clinical data including short history, age, gender, parity, lab tests, ultrasound report and macroscopy were recorded during surgery. Histopathology reports collected later. Total of 112 patients with mean age 42.6 years (range 22-82), 74 of whom were female. Most of them (46.42%) were asymptomatic. Single polyp was in 69, multiple in 32 and polyp with stone in 8 patients. Sessile polyp was 74.10%. Average polyp size was 7.6mm. Cholesterol polyp was in 82 patients. Four out of 5 malignant polyps were single and sessile. Abdominal ultrasound is the mainstay of diagnosis of gallbladder polyp but size, location, morphology, number and presence of associated gallstone has to be mentioned. Symptomatic gallbladder polyp benefited from surgery. Polyps more than 6mm, single and sessile morphology above the age 50 should undergo cholecystectomy.

Orbital cholesterol granuloma with destruction of the lateral orbital roof.

PURPOSE: Orbital cholesterol granuloma in a 51-year-old man is described. METHODS: Computed tomography (CT) and magnetic resonance imaging (MRI) were done. RESULTS: Both studies showed a mass in the left orbit, with evidence of orbital roof destruction in the CT scan. On the basis of clinical and imaging findings, a diagnosis was made of malignant orbital tumor with destruction of the lateral orbital roof. Surgical exploration revealed a thickly encapsulated mass densely adherent to the left superior orbital bone and periosteum. Although the dura mater was intact, bone destruction in the lateral orbital roof was seen. The entire mass was successfully excised and histopathological evaluation was performed. Histopathology showed numerous inflammatory cells, blood degradation products, and cholesterol clefts. The absence of epithelial elements led to the diagnosis of cholesterol granuloma. CONCLUSIONS: Care must be taken to differentiate cholesterol granuloma from malignant orbital tumor. CT scan and MRI imaging seem well-suited to detecting the characteristic findings of cholesterol granuloma.

Cox-2 expression in retinoblastoma.

PURPOSE: Cox-2, a prostaglandin synthase, is overexpressed in colorectal cancers and is involved in angiogenesis as well as in tumorigenesis. In this study, we investigate the expression of Cox-2 in retinoblastoma. METHODS: Twenty-nine formalin-fixed retinoblastoma specimens were examined by the labeled-streptavidin-biotin method using anti-Cox-2 antibody. RESULTS: Cox-2 positive immunoreactions were observed in 28 (96%) of 29 retinoblastomas specimens. CONCLUSION: This preliminary study suggests the overexpression of Cox-2 in both differentiated and undifferentiated retinoblastoma and its possible role in tumorigenesis.

Eccrine adenocarcinoma of the lacrimal sac region.

Eccrine adenocarcinoma of the lacrimal sac region is described in a 48-year-old man. The case was first diagnosed as an adenocarcinoma and removed by dacryocystectomy, but unfortunately the neoplasm recurred after a period of 1 year. Examinations with periodic acid-Schiff (PAS) and several antibodies indicate that this is a hitherto undescribed eccrine adenocarcinoma, and finally the case was managed by orbital exenteration. This is the first case of eccrine adenocarcinoma of the lacrimal sac region to be documented in the world literature.

Demonstration of S-100 protein immunoreactivity in normal human retina and retinoblastoma.

Specimens of 24 enucleated eyes from patients with retinoblastomas in situ were examined by labelled streptavidin biotin (LSAB) method to ascertain the distribution of S-100 protein and compared with 28 normal developing eyes. Polyclonal anti-S-100 antiserum and monoclonal alpha and beta chain anti-S-100 antibodies were used in this study. In the normal retina a weak reaction was observed in astrocytes and ganglion cells at 24 gestational weeks (GW) and there was an increase in the intensity of staining with increasing age. In the morphologically normal retina with retinoblastoma, astrocytes, ganglion cells and Müller cells showed positive reactions for S-100 protein. Examined tumors showed S-100 protein-positive glial cells that were interpreted as reactive astrocytes. No reaction product was detected in the tumor cells. These findings support the concept that in the retinoblastoma, only glial cells are positive for S-100 protein.

Retinoblastoma: clinical and immunocytochemical observations.

The clinical features of three cases of retinoblastoma and the histopathological and immunocytochemical findings of the retinoblastoma specimens of these patients are described. The other eye of each patient was normal. There was no family history of retinoblastoma. Fundal examination disclosed white masses in the posterior segments of the eyes. B-scan ultrasonography showed echo dense areas in the masses. Orbital tomograms showed no evidence of tissue densities. There was neither extraocular extension nor optic nerve involvement. Immunocytochemistry of paraffin-embedded tissues of the neoplasms revealed immunoreactivity with antibodies against S-100 protein, glial fibrillary acidic protein(GFAP), vimentin, neuron-specific enolase(NSE) and bcl-2. S-100, GFAP and vimentin were positive only for glial elements(reactive astrocytes) and, NSE and bcl-2 for almost all tumor cells. These findings support the previous reports that the majority of retinoblastomas are sporadic. The results of this study also support the views that retinoblastomas are composed of neuron-committed cells.

Clinical and electron microscopic features of retinoblastoma.

A male child of 1-year, 6-month-old had a history of leukocoria of the left eye for approximately three months prior to admission into our facility. No abnormality was found in the right eye. There was negative family history of retinoblastoma. Ophthalmoscopy revealed a white mass extending from the supero-posterior part of the left globe to the posterior surface of the lens. Orbital tomograms showed no intraocular tissue densities in the mass but a B-scan ultrasound showed an echo dense area of the mass. Histopathologically areas of photoreceptor differentiation and Flexner-Wintersteiner rosettes were observed in the tumor mass by light microscope. Transmission electron microscopy disclosed the presence of prominent mitochondria on the luminal side of the cells forming rosettes and these were believed to be the component parts of the inner-segments of the photoreceptor cells. The results of this study indicate a predominant neuronal nature of the neoplastic cells with photoreceptor-like differentiation.

Mixed cell malignant melanoma of the ciliary body.

Malignant melanomas of the ciliary body are uncommon tumors and the ratio of occurrence in the ciliary body to that in the choroid is 1:10. These tumors may have a nodular or diffuse growth pattern or combination of the two. The authors recently encountered a malignant melanoma of the ciliary body. After evaluation of the results of clinical examination, computed tomography(CT) and magnetic resonance imaging(MRI) a tentative diagnosis of malignant melanoma of the ciliary body in the left eye was made and an enucleation was done. Histopathological examination revealed the case as a mixed cell malignant melanoma of the ciliary body. The patient was followed up for approximately one year with no signs of metastasis or recurrence.

Epitheloid cell malignant melanoma of the conjunctiva.

Primary malignant melanoma of the conjunctiva is an uncommon neoplasm comprising only 2% of the malignant tumors of the eye. The tumors are usually composed of epitheloid, spindle or mixed cells and classified according to the predominant cells. Recently we encountered a conjunctival malignant melanoma occurring in a man. After full clinical and laboratory investigations, a clinical diagnosis of malignant melanoma of the conjunctiva in the left eye was entertained. The tumor was resected under local anesthesia and upon histological examination, the case was confirmed as a conjunctival malignant melanoma. Approximately one month after resection, orbital exenteration was carried out. The patient was followed-up for more than a year with no signs of metastasis or recurrence.

Inflammatory pseudotumor of the lacrimal sac.

A case of inflammatory pseudotumor of the lacrimal sac is presented. The patient was first consulted for epiphora and swelling of the right lacrimal sac region. A mass was found on computed tomography (CT) and finally it was removed by dacryocystectomy. The diagnosis of inflammatory pseudotumor was confirmed by histopathological sections.

Correlation between the induction of micronuclei in bone marrow by benzene exposure and the excretion of metabolites in urine of CD-1 mice.

Male and female CD-1 mice received single oral doses of benzene (220, 440, and 880 mg/kg) and were pretreated with modifiers of the mixed-function oxidase enzyme activities. Urinary metabolites (MT) (0-24 and 24-48 hr) were quantified by high-performance liquid chromatography. The micronucleus test was performed at 30 h. The following pretreatments were used to correlate micronucleus formation and the excreted benzene MT: 3-Methylcholanthrene and beta-naphthoflavone led to a marked increase in micronuclei (MN) and MT, whereas phenobarbital caused a slight increase, and SKF-525A had no effect. MN and MT were decreased when benzene was administered by the ip route or toluene was given simultaneously. Females had a lower number of MN and excreted more unconjugated phenol than did males. Muconic acid, hydroquinone, and phenol glucuronide and MN correlated well. They were dependent on both the dose and route of administration of benzene, being most inducible by P-448 inducers, in males more than females. The administration of hydroquinone induced MN, but phenol or catechol (200, 250, and 150 mg/kg, po, respectively) did not, and none of these compounds yielded trans, trans-muconic acid, a benzene MT in urine. This study establishes that benzene myeloclastogenicity is a function of its metabolism and that quantification of urinary metabolites could provide reliable correlates of this effect in vivo.

trans,trans-Muconic acid, an open-chain urinary metabolite of benzene in mice. Quantification by high-pressure liquid chromatography.

A sensitive h.p.l.c. method is described which separated urinary metabolites from benzene-treated male CD-1 mice. Phenol, trans,trans-muconic acid and quinol in the 48 h urine accounted, respectively, for 12.8-22.8, 1.8-4.7 and 1.5-3.7% of the orally administered single dose of benzene (880, 440 and 220 mg/kg body wt.). Catechol occurred in trace amounts. Ascorbic acid was used to adjust urine pH and increase the extraction efficiency of metabolites, especially muconic acid. It allowed an accurate estimation of quinol by preventing its auto-oxidation. trans,trans-Muconic acid was identified and was unique to benzene as none was detected in urine of mice dosed orally with phenol, catechol or quinol (250, 150 and 200 mg/kg, respectively). The potential existence of a toxic benzene metabolite in the form of an aldehyde precursor of muconic acid in vivo is discussed.

Benzene myeloclastogenicity: a function of its metabolism.

Using the micronucleus test we have found no significant difference between germ-free and conventional (non-germ-free) male CD-1 mice gavaged twice with 440 or 880 mg benzene/kg. Hence, the higher myeloclastogenicity observed previously with the p.o. (4-6 times) than with the i.p. route of benzene administration was ruled out as being due to the involvement of gut flora in benzene biotransformation. Pretreatment of males with 3-methylcholanthrene or beta-naphthoflavone, inducers of P-448 monooxygenase, but not phenobarbital, an inducer of P-450, significantly enhanced the myeloclastogenic effect of a single oral dose of benzene (440 mg/kg). Single oral doses of phenol, catechol, or hydroquinone (250, 150, and 200 mg/kg, respectively) failed to reproduce the potent myeloclastogenic effect of benzene. In fact, only hydroquinone was mildly clastogenic. The relation between benzene's myeloclastogenicity and metabolism is discussed.

The influence of simple aromatics on benzene clastogenicity.

The micronucleus test was performed in male ICR Swiss mice following modification of benzene metabolism by co-administration of aniline, pyridine or naphthalene, or by prior injection of alpha-naphthoflavone. HPLC profiles of urinary metabolites were compared to the effects of these compounds on clastogenicity. Pyridine inhibited both benzene clastogenicity and its metabolism. Aniline and naphthalene increased the clastogenicity and slightly altered the metabolism of benzene. alpha-Naphthoflavone inhibited benzene clastogenicity and metabolism only at high doses. Since 3-methylcholanthrene and phenobarbital both increase the metabolism of benzene but only 3-methylcholanthrene increases benzene clastogenicity, specific P450 isozymes may be responsible for different biological effects of benzene, and alterations in these effects might be caused by a shift from one isozyme to another.

Modifications in the myeloclastogenic effect of benzene in mice with toluene, phenobarbital, 3-methylcholanthrene, Aroclor 1254 and SKF-525A.

Benzene was studied in its target organ of effect, the bone marrow, with the micronucleus test and metaphase analysis. Male and female CD-1 mice were treated with 2 doses of benzene (440 mg/kg) or toluene (860 or 1720 mg/kg) or both 24 h apart, and sacrificed 30 h (or 54 h) after the first dose. Benzene-treated animals were pretreated with phenobarbital (PB), 3-methylcholanthrene (3-MCA), SKF-525A, or Aroclor 1254. Toluene showed no clastogenic activity and reduced the clastogenic effect of benzene when the mixture was given. None of the pretreatments protected against the clastogenic effect of benzene. 3-MCA pretreatment greatly promoted benzene myeloclastogenicity. Females were consistently more resistant to benzene than males. Dose-response curves in benzene-treated mice were much steeper with 3-MCA induction than without. Chromosomal damage was higher with p.o. than i.p. benzene administration.