Biomedical subjects
Publications and source records attributed to K Suda.
The ATP-dependent proteases Clp and FtsH from bacteria, as well as mitochondrial homologs of FtsH and Lon from yeast, may act as chaperones; they mediate not only proteolysis, but also the insertion of proteins into membranes and the disassembly or oligomerization of protein complexes. The coordination of such processes with selective proteolysis may function in the quality control of protein biogenesis.
We investigated 47 autopsy cases of metastatic cancer involving the pancreas. Metastatic disease in nine cases involved the pancreatic duct epithelium. In two cases, metastatic cancer cells showed Pagetoid features. In three cases, pancreatic metastatic disease showed solitary proliferation with focal in situ carcinoma-like lesions mimicking primary pancreatic cancers. Each of these three cases had primary lung adenocarcinomas. Serial sections revealed abrupt borders between the in situ carcinoma-like lesions and the non-cancerous epithelium. Primary pancreatic cancers did not show Pagetoid features or abrupt borders between the cancerous and non-cancerous epithelium. We conclude that the possible diagnosis of pancreatic metastasis should be carefully ruled out in the histological detection of latent primary pancreatic cancer.
In autopsy specimens removed after gastrectomy from patients who had survived for 2.5 to 40 years after surgery, we found hyalinization of the islets of Langerhans in 9 of 15 cases (60%) with Billroth's I anastomosis (B-I) and in 8 of 16 cases (50%) with Billroth's II anastomosis (B-II). The hyalinization in the postgastrectomy patients was significantly increased compared with that in controls (p < 0.01). The percentage of hyalinized islets of Langerhans in the 17 cases showing hyalinization ranged from 0.2% to 14.3%. The percentage increased relative to the period after gastrectomy in the B-I patients but not in those with B-II. The blood glucose level was mildly elevated in three B-I patients, whereas it was increased in only one patient with B-II. Hyalinization of the islets of Langerhans may be due to vagotomy or to excessive stimulus and hyperactivation of the islets. In any event, the islets of Langerhans in patients after gastrectomy were frequently replaced by hyalinization, which might cause impaired glucose tolerance.
Hyperostosis is a well-known bony reaction associated with meningioma. However, it is difficult to determine preoperatively whether meningioma cells have invaded the bone, and if so, the extent of tumor invasion. Preoperative thallium-201 chloride single photon emission computed tomography (201Tl SPECT) was performed in four patients with meningioma and hyperostosis. The presence of meningioma cells in bone biopsy specimens was also investigated using standard histological techniques. 201Tl SPECT revealed increased uptake in three of the four patients. Biopsy specimens from these three patients revealed invasion of the bony lesions by meningioma cells in accordance with the 201Tl SPECT findings. 201Tl SPECT found no abnormal uptake in the other patient, in which there was also no histological evidence of tumor invasion of bone. Preoperative 201Tl SPECT can provide information on bone invasion by meningioma, which will facilitate preoperative planning of the extent of bony resection required at meningioma surgery.
We report a 70-year-old man with progressive gait disturbance and gaze palsy. The patient was well until summer of 1991 when he was 66-year-old, when he noted a gradual onset of difficulty in gait and looking downward. He was evaluated in our hospital in May, 1994 when he was 69-year-old. On admission, he was alert but markedly demented with disorientation and memory loss. Constructional apraxia and dressing apraxia were noted. He had difficulty in gaze to all directions; he could move his eyes only 20% of the normal range. Oculocephalic response was retained. He had small voice and some dysphagia. Other cranial nerves were unremarkable. He could not walk unsupported. Marked retropulsion was noted in which he would fell down spontaneously upon standing unless supported. Moderate to marked rigidity was noted in the neck, trunk, and in the legs, however, in the upper extremities, rigidity was only mild. No tremor was noted. Deep reflexes were symmetrically exaggerated with ankle clonus bilaterally. Plantar response was flexor. Sensation was intact. Routine laboratory tests were unremarkable, however, his cranial MRI showed moderate to marked fronto-temporal atrophy and moderate midbrain and pontine tegmental atrophy. The third ventricle was markedly dilated. He was discharged for out patient care, however, his dysphagia had become progressively worse, and he suffered from frequent bouts of pneumonia. He was admitted to our service on October 17, 1994. His neurologic examination was essentially similar except that he showed more advanced dementia. He was still able to stand with support. Gastrostomy was placed on October 25. Post-operative course was unremarkable. He was discharged on November 1. His motor disturbance showed gradual deterioration, and by the May of 1995, he became bed-ridden, and was admitted to another hospital on May 30, 1995. He was almost totally unable to move his eyes, but oculocephalic response was still elicited. Marked truncal and limb rigidity were noted. He vomited coffee-ground substance on October 31, 1995, and developed hypotension. The subsequent course was complicated by pneumonia and he expired on November 24. The patient was discussed in a neurological CPC. Majority of the participants thought that the patient had progressive supranuclear palsy, but some participants thought that the patient had corticobasal degeneration because cortical atrophy was so marked. Post mortem examination revealed atrophy of the frontal and parietal lobe. The brain stem was atrophic particularly in the tegmental area including the midbrain. The substantia nigra showed marked neuronal loss and globose type neurofibrillary tangles in the remaining neurons. The neurons in the locus coeruleus was well retained, however neurofibrillary tangles were seen. In addition, the cerebellar dentate nucleus, the inferior olivary nucleus, and the internal globus pallidus showed marked neuronal loss and neurofibrillary degeneration. In the frontal cortex, although macroscopic examination showed some atrophy, microscopic examination failed to show neuronal loss or gliosis. The pathologic findings were consistent with the diagnosis of progressive supranuclear palsy.
Pancreatic intralobular fibrosis in liver cirrhotic patients was studied immunohistochemically using alpha-smooth muscle actin (alpha SMA). Similarly micronodular arrangements of acinar cells and hypertrophy of Langerhans' islands in liver cirrhotic patients were studied using proliferating cell nuclear antigen (PCNA). In addition, pancreata in liver cirrhotic patients were studied from apoptotic side. We investigated the histopathologic autopsy findings of 103 patients: 15 patients with alcoholic liver cirrhosis, 49 patients with non-alcoholic liver cirrhosis and, as controls, 39 patients without a history of alcohol abuse or liver dysfunction. alpha SMA positive area ratio and PCNA positive cell ratio in liver cirrhotic patients were higher than in the controls. In contrast, apoptotic cell ratio in liver cirrhotic patients was lower than in the controls. alpha SMA positive area ratio in patients with pancreatic intralobular fibrosis was higher than in patients without pancreatic intralobular fibrosis. PCNA positive cell ratio in patients with micronodular arrangements of the acinar cells was higher than in patients without micronodular arrangements of the acinar cells. We conclude that pancreata in liver cirrhotic patients are predominant of proliferating changes.
We report a 64-year-old woman who developed nausea, headache, and consciousness disturbance. She was well until four years before the onset of her neurologic illness when (April of 1990 at her 59 years of the age) she was found to have an early cancer in her anterior wall of the lower stomach. Subtotal gastrectomy was performed and the operative result was reported as curative. Four years after the surgery (December of 1994 at her 64 years of the age), she noted suboccipital headache and nausea which had become progressively worse and she was admitted to our service on May 24, 1995. On admission, she appeared chronically ill but general physical examination was unremarkable with normal vital signs. Neurologically she was alert and not demented, and the higher cerebral functions were intact. Cranial nerves were also unremarkable. She was able to walk in tandem and on heels. No motor weakness or ataxia was noted. Deep tendon reflexes were moderately increased, however, no Babinski sign was noted. Although she had headache, no meningeal signs were seen. Slight superficial and vibratory sensory loss was noted in both feet. Routine blood work was again unremarkable except for slight increase in CEA to 8.3 ng/dl (N < 5 ng/dl). The opening pressure of lumbar CSF was 180 mm H2O and the CSF contained 39 cells/microliter, 79 mg of protein, and 10 mg/dl of glucose. Approximately half of the cells were atypical malignant cells. Plain CT was unremarkable, however, tentorial border showed enhancement after contrast infusion. FGS showed no malignant tumors in the stomach. She was treated with intravenous glycerol and whole brain radiation, however, she continued to complain of severe headache, and her sensorium started to be disturbed one month after the admission. Follow-up cranial CT scan revealed enlargement of the lateral and the third ventricles. Her consciousness progressively deteriorated and she became comatose three months after the admission. Repeated cranial CT scan showed enlargement of the ventricles, but no mass lesions were seen within the brain. She developed respiratory arrest on September 25 of the same year. She was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had a gastric cancer with meningeal seeding developing meningeal carcinomatosis. The cause of deep coma was ascribed to damage of cerebral cortical areas secondary to metastatic carcinoma cells and fibrinous materials in the surface of the brain. Postmortem examination revealed thickening and clouding of leptomeninges of the cerebral convexity. On histologic observation, patchy areas of fibrous thickening were seen in the cerebral leptomeninges; in such areas, adenocarcinomatous cells were seen scattered. The basal meninges were free of carcinoma cells, however, leptomeninges of the cerebellum and brain stem tegmentum contained scattered carcinoma cells. The lateral and the third ventricles were enlarged, however, insides of the brain were free of pathologies; the ependymal layer were intact. In the stomach no carcinoma cells were remaining. Pneumonic changes were seen in the right upper and the left lower lobes which appeared to be the direct cause of her death. No evidence of tentorial herniation was noted. The cause of her deep coma was not clearly determined, however, combination of hydrocephalus and cortical malfunction due to leptomeningeal carcinoma cell infiltration and fibrinous material accumulation appeared to have played a role.
OBJECTIVE: To evaluate the mechanism of localized portal hypertension associated with stenosis or obstruction of the splenic vein in chronic alcoholic pancreatitis. DESIGN: Surgical and autopsy specimens from 12 patients with clinically diagnosed chronic alcoholic pancreatitis were examined histopathologically. Autopsy specimens of 10 normal pancreases served as control tissues. RESULTS: In tissues from 11 of the 12 patients with chronic-alcoholic pancreatitis, fibrosis in the pancreatic parenchyma continuously extended to the wall of the splenic vein; organized thrombus formation with recanalization was found in five patients, phlebosclerosis in four, and no changes were found in two. In two of the five patients with organized thrombus formation in the splenic vein, localized portal hypertension had been clinically diagnosed because of splenomegaly and varicose veins in the fundus of the stomach, but it was not accompanied by liver cirrhosis. In the control tissues, fibrosis was not observed in the peripancreatic tissue or the area surrounding the wall of the splenic vein. CONCLUSION: We regard localized portal hypertension due to stenosis or obstruction of the splenic vein as one of the consequences of peripancreatic fibrosis in chronic alcoholic pancreatitis.
We report a 85-year-old woman who died after one year history of convulsion, dementia, and consciousness disturbance. She was apparently well until January 6, 1995 when she was 85 year old; on that evening, she suddenly stated that some one was in her room and she became confused. A local MD gave her diazepam and she fell into sleep. At 3 o'clock in the following morning, she developed tonic-clonic convulsion in her right lower extremity which showed a march to her right upper extremity and the left lower extremity. She was admitted to our hospital. On admission, she was comatose with respiratory acidosis. She was intubated and placed on a ventilator. She was treated with intravenous phenytoin. She gradually gained consciousness and became alert. Respiration became normal. Her MRI revealed ventricular dilatation, fronto-parietal cortical atrophy, and a T1-low and T2-high signal intensity lesion in the left occipital lobe. She was discharged for out patient follow-up on February 4, 1995. Since then, she noted loss of memory and small step gait. A follow-up CT scan revealed a mass lesion which showed a ring-shaped enhancement in the left occipital lobe and was admitted again. On admission, she was alert but markedly demented. The optic fundi was unremarkable, but she appeared to have right homonymous hemianopsia. No motor weakness was noted. In Gd-DTPA enhanced MRI, the above tumor showed a ring enhancement. The diagnosis of glioblastoma was entertained, however, considering her age, she was treated with intravenous glycerol and intramuscular steroid. She was discharged for out-patient follow-up on July 15, 1995. Her gait disturbance had progressively become worse and she developed nausea and vomiting and was admitted again on October 2, 1995. On admission, she was somnolent and markedly demented. Brain stem responses were retained normally. She was unable to stand or walk. Deep tendon reflexes were slightly increased in the right upper extremity and the plantar response was extensor on the right. Her hospital course was complicated by respiratory tract infection and respiratory acidosis. She expired on November 2, 1995. The patient was discussed in a neurological CPC and the chief discussant arrived at the conclusion that she had a glioblastoma involving the left occipital lobe and the adjacent areas. Post-mortem examination revealed an infiltrating tumor in the left occipital lobe. On microscopic examination, the tumor was very cellular; nuclear atypism was marked and tumor cells undergoing mitosis were seen. In some areas, capillary proliferation was seen. Histologic characteristics were consistent with glioblastoma.
Multinucleated giant cells in the pancreas (five giant cell carcinomas, a mucinous cystadenocarcinoma attended with many osteoclast-like giant cells, 42 invasive ductal carcinomas and 29 chronic pancreatitises) were examined. Three types of multinucleated giant cell were identified: epithelial type, coexpressive type, mesenchymal type. Epithelial type expressed epithelial markers, such as keratin and EMA in 23 ductal carcinomas. Coexpressive type expressed both epithelial markers and mesenchymal marker vimentin was in four ductal carcinomas. Mesenchymal type expressed mesenchymal markers, vimentin and CD68 in four osteoclastoid type giant cell carcinomas, the mucinous cystadenocarcinoma, six ductal carcinomas and ten chronic pancreatitises. Epithelial and coexpressive type were considered to be epithelial neoplastic origin, those had bizarre appearance and transitional area from definite adenocarcinoma area. Vimentin expression is associated with sarcomatous proliferation. Mesenchymal type was considered to be nonneoplastic and a certain type of macrophage polykaryons.
We report a 65-year-old man with progressive loss of vision and consciousness disturbance. The patient was well until his age of 63 when he was found to have a gastric cancer. He was treated by the tumor resection and chemotherapy; he was apparently well, but hepatic metastases were found in the next year (1996). In June, 1996, he noted an onset of blurred vision more on the left. He was admitted to the ophthalmology service of our hospital on July 14, 1996. His vision was 0.8 on the right and 0.15 on the left. He was treated with oral prednisolone with slight improvement. He was also found to have IgM kappa-type monoclonal gammopathy; Bence-Jones protein was positive and a bone marrow aspiration revealed that approximately 10% of bone marrow cells were atypical plasma cells. His vision had progressively got worse and he became blind by the end of October 1996. A chest X-ray and cranial CT scan revealed multiple abnormal nodular densities. In the middle of November 1996, he became confused, disoriented and agitated. His mental symptoms had progressively became worse, and a neurologic consultation was asked on December 10, 1996. Neurologic examination revealed that he was somnolent with decreased attention to his surroundings. He showed marked disorientation and memory loss. Higher cerebral functions appeared intact. He was able to recognize only light and dark. Pupils were moderately dilated with very sluggish light reflex remained. Vertical gaze was moderately restricted and horizontal nystagmus was noted upon left and right lateral gaze. The remaining of the neurologic examination were unremarkable. General physical examination revealed hepatosplenomegaly; the liver was palpable by 3 cm below the right costal margin. Laboratory examination revealed anemia (Hb10.1 g/dl) and thrombocytopenia (43,000/microliter). A cranial CT scan and MRI revealed a mass lesion in involving the chiasmatic and bilateral hypothalamic areas. The tumor showed intense homogeneous enhancement after Gd-DTPA infusion. The patient was treated with dexamethasone and radiation. After 9 Gray radiation, he showed deterioration in the sensorium; a cranial CT scan revealed a hydrocephalus of the right ventricle with the midline shift towards left. The radiation was discontinued. The subsequent clinical course was complicated by aspiration pneumonia and thrombocytopenia. He expired on January 4, 1997. The patient was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had systemic malignant lymphoma with metastasis to the brain judging from the characteristics of MRI and CT findings. Opinions were divided between malignant lymphoma and metastatic brain tumor. Post-mortem examination revealed plasmacytoid lymphocytic infiltration in the bone marrow. Immunologically, these cells were positive for IgM and kappa-type light chain. These plasmacytic infiltrations were seen in the lungs and lymph nodes. These findings were consistent with the diagnosis of Waldenström's macroglobulinemia. In the liver metastatic cancer tissues were seen; microscopic pictures were essentially similar to those of resected gastric cancer. No local recidive was noted in the stomach. In the central nervous system, a necrotic tissue was involving the hypothalamic area bilaterally; no clear neoplastic cells were found, however, lymphocytic and plasmacytic infiltrations were seen in the perivascular space. In the optic nerves, loss of myelin and axons were seen. These findings most likely mass formation from macroglobulinemia which underwent necrotic change after radiation. Mass formation in the brain is rare for Waldenström's macroglobulinemia, although it has been reported. The relation between gastric cancer and macroglobulinemia in this patient is unclear.
We report a 62-year-old man who developed coma and died in a fulminant course. The patient was well until May 1, 1996 when he noted chillness, tenderness in his shoulders, and he went to bed without having his lunch and dinner. In the early morning of May 2, his families found him unresponsive and snoring; he was brought into the ER of our hospital. He had histories of hypertension, gout, and hyperlipidemia since 42 years of the age. On admission, his blood pressure was 120/70, heart rate 102 and regular, and body temperature 36.3 degrees C. His respiration was regular and he was not cyanotic. Low pitch rhonchi was heard in his right lower lung field. Otherwise general physical examination was unremarkable. Neurologic examination revealed that he was somnolent and he was only able to respond to simple questions such as opening eyes and grasping the examiner's hand, but he was unable to respond verbally. The optic discs were flat; the right pupil was slightly larger than the left, but both reacted to light. He showed ptosis on the left side, conjugate deviation of eyes to the left, and right facial paresis. The oculocephalic response and the corneal reflex were present. His right extremities were paralyzed and did not respond to pain Deep tendon reflexes were exaggerated on the right side and the plantar response was extensor on the right. No meningeal signs were present. Laboratory examination revealed the following abnormalities; WBC 18,400/ml, GOT 131 IU/l GPT 50 IU/l, CK616 IU/l, BUN 30 mg/dl, Cr 2.1 mg/ dl, glucose 339 mg/dl, and CRP 27.4 mg/dl. ECG showed sinus tachycardia and ST elevation in II, III and a VF leads and abnormal q waves in I, V5, and V6 leads. Chest X-ray revealed cardiac enlargement but the lung fields were clear. Cranial CT scan revealed low density areas in the left middle cerebral and left posterior cerebral artery territories. The patient was treated with intravenous glycerol infusion and other supportive measures. At 2: 10 AM on May 3, he developed sudden hypotension and cardiopulmonary arrest. He was pronounced dead at 3:45 AM. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that the patient had acute myocardial infarction involving the inferior and the true posterior walls and left internal carotid embolism from a mural thrombus. Post mortem examination revealed occlusion of the circumflex branch of the left coronary artery due to atherom plaque rupture and myocardial infarction involving the posterior and the lateral wall with a rupture in the postero-lateral wall. Marked atheromatous changes were seen in the left internal carotid, the middle cerebral and the basilar arteries; the left internal carotid and the middle cerebral arteries were almost occluded by thrombi and blood coagulate. The territories of the left middle cerebral and the occipital arteries were infarcted; but the left thalamic area was spared. The neuropathologist concluded that the infarction was thrombotic origin not an embolic one as the atherosclerotic changes were severe. Cardiac rupture appeared to be the cause of terminal sudden hypotension and cardiopulmonary arrest. It appears likely that a vegetation which had been attached to the aortic valve induced thromboembolic occlusion of the left internal carotid artery which had already been markedly sclerotic by atherosclerosis. It is also possible that the vegetations in the aortic valve came from mural thrombi at the site of acute myocardial infarction, as no bacteria were found in those vegetations.
Afg3p and Rca1p are adenosine triphosphate (ATP)-dependent metalloproteases in yeast mitochondria. Cells lacking both proteins exhibit defects in respiration-dependent growth, degradation of mitochondrially synthesized proteins, and assembly of inner-membrane complexes. Defects in growth and protein assembly, but not in degradation, were suppressed by overproduction of yeast mitochondrial Lon, an ATP-dependent serine protease. Suppression by Lon was enhanced by inactivation of the proteolytic site and was prevented by mutation of the ATP-binding site. It is suggested that the mitochondrial proteases Lon, Afg3p, and Rca1p can also serve a chaperone-like function in the assembly of mitochondrial protein complexes.
BACKGROUND: Superficial-type early colorectal carcinoma (SCa) is presently not a rare finding and is very important in discussions regarding the development of large bowel cancers, although the histologic characteristics of SCa remain obscure. METHODS: Using 54 SCa lesions (34 intramucosal adenocarcinomas (SCa-m) and 20 adenocarcinomas with invasion to the submucosa (SCa-sm)), the largest dimension of the depressed region of the lesion and the greatest dimension of the entire lesion were measured by the computed image analyzer, and the expression of p53 and ras of SCa were examined immunohistochemically. RESULTS: The percent of depressed regions in SCa lesions measuring less than 5 mm in greatest extent was larger than in those measuring more than 6 mm, and the percent of depressed regions in SCa-sm with deeper carcinoma invasion was lower than that of SCa-sm with shallower invasion. There was a positive correlation between the depth of invasion and the maximum dimension of the carcinoma. The frequency of association with adenoma in all SCa-m was 21% and was 32% in SCa-m that were more than 6 mm in greatest extent, although all minute SCa-m lesions less than 5 mm were pure carcinomas without any adenomatous component. Positive expression of ras was noted in 41% of SCa-m and 36% of SCa-sm, respectively, while positive expression of p53 was noted in 63% of SCa-m and 88% of SCa-sm, respectively. CONCLUSIONS: These results suggested that 70% to 80% of SCa developed via a de novo carcinoma theory and showed the depression form in the initial histologic stage and thereafter in the flat-protrusion form, while 20% to 30% of SCa arose from the preexisting flat adenoma via the adenoma-carcinoma sequence theory. The results also suggested that p53 was related to the enlargement and deeper invasion of SCa, regardless of the sequence of development of colorectal cancer.
We examined the primary ischaemic changes in the pancreas in 35 patients with disseminated intravascular coagulation. In 7 (20%), multiple patchy lesions composed of degenerative acinar cells indicating coagulation necrosis were noted. None of these lesions was accompanied by fat necrosis. The patchy lesions involved the islets of Langerhans in only 1 case. The interlobular arteries of the pancreas near these lesions contained fibrin thrombi in all 7 cases. We suggest that these lesions, without fat necrosis, are the distinctive ischaemic change associated with disseminated intravascular coagulation.
CONCLUSION: The results suggest that systemic administration (s.c. and i.p.) of BOP induces liver damage due to BOP itself and/or its metabolites which might be formed in the liver and that interaction of BOP itself in the pancreatic duct with pancreatic juice plays an important role for pancreatic duct tumorigenicity. METHODS: Mutagenic activation and pancreatic duct tumorigenicity of N-nitrosobis (2-oxopropyl)amine (BOP) administered s.c., i.p., and i.d. were studied in dogs. RESULTS: Following i.p. administration of BOP, N-nitroso(2-hydroxypropyl) (2-oxopropyl)amine (HPOP) and N-nitrosobis(2-hydroxypropyl)amine (BHP), but not BOP, were detected in pancreatic juice, while following i.d. administration, only BOP was detected. The pancreatic juice of one dog that received 100 mg of BOP i.d. showed positive mutagenicity towards Salmonella typhimurium TA100, but the pancreatic juice of two dogs that received 100 mg of BOP i.p. was not mutagenic. BOP showed clear mutagenicity in the presence of pancreatic juice from untreated dogs, but the pancreatic juice could not activate HPOP and BHP to mutagens. BOP administered sc for 2 wk (total dose: 600 mg) induced clinical toxicity, nausea, vomiting, and loss of appetite at 10 wk. BOP administered i.p. for 4 mo (total dose: 2000 mg) induced liver damage at 6 mo, but no pancreatic injury. BOP administered i.d. for 6.5 or 12 mo (total dose: 2500 or 4700 mg, respectively) induced papillary hyperplasia and dysplasia of duct epithelial cells and ductal proliferation with fibrosis.
The distribution and clinicopathologic features of pancreatic fibrosis were studied histopathologically in 137 autopsy cases of chronic alcohol abuse. Fibrosis was observed in 90 of the cases and was classified as perilobular sclerosis (PS) and intralobular sclerosis (IS). Fibrosis of the PS type was irregular and sometimes patchy and extended into the intralobular area in advanced cases. In some advanced cases, complete replacement of the pancreatic tissue by extensive fibrosis was seen. Fibrosis of the IS type was uniformly distributed. The tissues in some cases showed prominently periacinar fibrosis. In these cases, the pancreatic parenchyma had not been completely replaced by extensive fibrosis. Clinicopathologic comparisons revealed the following results: accompanying liver cirrhosis was greater in the IS than in the PS of fibrosis. However, a higher frequency of protein plugs, pancreatic stones, extensive fibrosis replacement, peripancreatic fibrosis, splenic vein involvement, choledochus involvement, pseudocyst, and ductal hyperplasia was found in the PS type compared to the IS type. In conclusion, the findings on the perilobular and intralobular distribution of fibrosis and differences in various components or accompanying diseases in pancreatic fibrosis suggest that this entity shows two distinct pathologic patterns with differing mechanisms.
We have investigated 44 cases of duodenal diverticulum to delineate the pathological features. Foamy cell aggregations were observed in 24 (54.5%) of the cases. The foamy cells were located within the submucosa in all 24 cases and were found around the deepest portion of the diverticula in 14. There were no statistically significant differences between the depth of the diverticulum and the presence or degree of foamy cell aggregation. Lymphoid aggregates, focal thickening of the muscularis mucosae, submucosal fibrosis, intimal thickening of submucosal vessels and submucosal haemorrhage were also detected, but statistical analysis showed no significant associations between these pathological findings and the presence of foamy cell aggregates. We conclude that the foamy cell aggregates are a non-specific but frequent pathological finding in duodenal diverticula and which have not been described in previous studies.