The National High Blood Pressure Education Program presents the complete Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Like its predecessors, the purpose is to provide an evidence-based approach to the prevention and management of hypertension. The key messages of this report are these: in those older than age 50, systolic blood pressure (BP) of greater than 140 mm Hg is a more important cardiovascular disease (CVD) risk factor than diastolic BP; beginning at 115/75 mm Hg, CVD risk doubles for each increment of 20/10 mm Hg; those who are normotensive at 55 years of age will have a 90% lifetime risk of developing hypertension; prehypertensive individuals (systolic BP 120-139 mm Hg or diastolic BP 80-89 mm Hg) require health-promoting lifestyle modifications to prevent the progressive rise in blood pressure and CVD; for uncomplicated hypertension, thiazide diuretic should be used in drug treatment for most, either alone or combined with drugs from other classes; this report delineates specific high-risk conditions that are compelling indications for the use of other antihypertensive drug classes (angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, beta-blockers, calcium channel blockers); two or more antihypertensive medications will be required to achieve goal BP (<140/90 mm Hg, or <130/80 mm Hg) for patients with diabetes and chronic kidney disease; for patients whose BP is more than 20 mm Hg above the systolic BP goal or more than 10 mm Hg above the diastolic BP goal, initiation of therapy using two agents, one of which usually will be a thiazide diuretic, should be considered; regardless of therapy or care, hypertension will be controlled only if patients are motivated to stay on their treatment plan. Positive experiences, trust in the clinician, and empathy improve patient motivation and satisfaction. This report serves as a guide, and the committee continues to recognize that the responsible physician's judgment remains paramount.

Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure

Viral hepatitis in all its forms is a major public health problem throughout the world, affecting several hundreds of millions of people. Viral hepatitis is a cause of considerable morbidity and mortality both from acute infection and chronic sequelae which include, in the case of hepatitis B, C and D, chronic active hepatitis and cirrhosis. Hepatocellular carcinoma, which is one of the 10 commonest cancers worldwide, is closely associated with hepatitis B and, at least in some regions of the world, with hepatitis C virus. This timely monograph is a distillation of knowledge of hepatitis B, C and D, based on a review of 1000 studies by a small group of scientists. (It is interesting to note in passing that some 5000 papers on viral hepatitis are published annually in the world literature.) The epidemiological, clinical and experimental data on the association between infection with hepatitis B virus and primary liver cancer in humans are reviewed in a readable and succinct format. The available information on hepatitis C and progression to chronic infection is also evaluated and it is concluded (perhaps a little prematurely) that hepatitis C virus is carcinogenic. However, it is concluded that hepatitis D virus, an unusual virus with a number of similarities to certain plant viral satellites and viroids, cannot be classified as a human carcinogen. There are some minor criticisms: there are few illustrations and some complex tabulations (for example, Table 6) and no subject index. A cumulative cross index to IARC Monographs is of little value and occupies nearly 30 pages. This small volume is a useful addition to the overwhelming literature on viral hepatitis, and the presentation is similar to the excellent World Health Organisation Technical Reports series on the subject published in the past. It is strongly recommended as a readable up-to-date summary of a complex subject; and at a cost of 65 Sw.fr (approximately £34) is excellent value. A J ZUCKERMAN

https://jcp.bmj.com/content/jclinpath/48/7/691.1.full.pdf

IARC Monographs on the Evaluation of Carcinogenic Risks to Humans

Background and Purpose—This scientific statement provides an overview of the evidence on vascular contributions to cognitive impairment and dementia. Vascular contributions to cognitive impairment ...

Vascular Contributions to Cognitive Impairment and Dementia A Statement for Healthcare Professionals From the American Heart Association/American Stroke Association

Summary The term cerebral small vessel disease refers to a group of pathological processes with various aetiologies that affect the small arteries, arterioles, venules, and capillaries of the brain. Age-related and hypertension-related small vessel diseases and cerebral amyloid angiopathy are the most common forms. The consequences of small vessel disease on the brain parenchyma are mainly lesions located in the subcortical structures such as lacunar infarcts, white matter lesions, large haemorrhages, and microbleeds. Because lacunar infarcts and white matter lesions are easily detected by neuroimaging, whereas small vessels are not, the term small vessel disease is frequently used to describe the parenchyma lesions rather than the underlying small vessel alterations. This classification, however, restricts the definition of small vessel disease to ischaemic lesions and might be misleading. Small vessel disease has an important role in cerebrovascular disease and is a leading cause of cognitive decline and functional loss in the elderly. Small vessel disease should be a main target for preventive and treatment strategies, but all types of presentation and complications should be taken into account.

https://www.thelancet.com/pdfs/journals/laneur/PIIS1474-4422(10)70104-6.pdf

Cerebral small vessel disease: from pathogenesis and clinical characteristics to therapeutic challenges.

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Pathology and genetics of tumours of the digestive system

Nine acinar cell carcinomas of the pancreas, 2 pancreatoblastomas, 16 solid-cystic (papillary-cystic) tumors, and 20 ductal adenocarcinomas were immunocytochemically investigated using antisera against four pancreatic enzymes (alpha-amylase, lipase, trypsinogen, chymotrypsinogen), four pancreatic hormones, neuron specific enolase (NSE), alpha-1-antitrypsin (AAT), carcinoembryonic antigen (CEA), and CA 19–9. Lipase, trypsinogen, and chymotrypsinogen, but no alpha-amylase were detected in all acinar cell carcinomas and pancreatoblastomas. In contrast, solid-cystic tumors (SCT) were negative for pancreatic enzymes but 2 of 16 stained with NSE. No neuroendocrine granules or pancreatic hormones could be demonstrated. AAT was found in all tumors except ductal adenocarcinomas, which stained with CEA and CA 19–9. The study established pancreatic enzymes (except alpha-amylase) as immunocytochemical markers for acinar cell carcinomas and pancreatoblastomas. There is as yet no marker specific for SCT, which would elucidate the obscure histogenetic origin and phenotypic differentiation of these tumors. Cancer 59:729-747, 1987.

Immunocytochemical markers of uncommon pancreatic tumors. Acinar cell carcinoma, pancreatoblastoma, and solid cystic (papillary-cystic) tumor.

Two cases of infantile carcinoma of the pancreas were diagnosed as pancreatoblastoma based on the morphogenesis of the tumors. These encapsulated tumors adhered to the head of the pancreas and to the descending portion of the duodenum. Histologic examination revealed an organoid structure made up of cords or nodules of squamoid cells with elongated nuclei arranged in a parallel fasciculating pattern (squamoid corpuscles), surrounding tubular structures of columnar epithelial cells and intermediate light cell masses with little differentiation. Electron microscopy revealed zymogen-like granules and well developed granular endoplasmic reticulum in the cytoplasm. There were no detectable islet cells in tumor tissue. Both of these tumors could be derived from the ventral pancreas and be isolated by the lack of communication with the duct of Wirsung. As the duct of Santorini was patent, extirpation of these organoid tumors would not influence secretion of pancreatic juice. Considering the favorable prognosis after extirpation of these tumors, they should be differentiated from the usual adenocarcinoma of the pancreas occurring in adults.

Morphogenesis of pancreatoblastoma, infantile carcinoma of the pancreas. Report of two cases

We examined sclerotic changes of the medullary arteries in 110 nonneuropsychiatric patients ranging in age from the second to the ninth decades, in 20 patients with subcortical arteriosclerotic encephalopathy (Binswanger's disease), and in 20 patients with dementia of the Alzheimer type. The principal sclerotic change was fibrohyaline thickening of the wall, which began to appear during the late fourth decade, increased in incidence gradually with age, and was most severe in patients with subcortical arteriosclerotic encephalopathy. Morphometry showed that the sclerotic changes of the medullary arteries were most prominent in the frontal lobe, followed by the parietal, occipital, and temporal lobes, in both the nonneuropsychiatric and demented groups. The sclerotic rate in the frontal lobe of patients with dementia of the Alzheimer type was slightly higher than that in the nonneuropsychiatric patients (p less than 0.05) but far less than that in the patients with subcortical arteriosclerotic encephalopathy (p less than 0.001). The sclerotic rate correlated well with the degree of ischemic white matter changes as well as with blood pressure.

Medullary arteries in aging and dementia.

Six cases of primary hepatic carcinomas with a significant amount of sarcomatoid elements were examined by using immunohistochemical stainings. Four of the six cases were associated with ordinary hepatocellular carcinoma (HCC), one with cholangiocellular carcinoma (CCC), and one with mixed HCC and CCC. Alpha-fetoprotein and alpha-1-antitrypsin were negative in sarcomatoid cells of all cases; vimentin stained positively in sarcomatoid tumor cells in two of the six cases; and cytokeratin (CK8) was detected in five cases. The CK8 was not detected in tumor cells of two cases of hepatic angiosarcoma, two of metastatic leiomyosarcomas, and one of metastatic fibrosarcoma, although vimentin stained positively in all these true sarcomas. It was concluded that sarcomatoid dedifferentiation of liver carcinomas might derive from both HCC and CCC. In addition CK8 might be an excellent marker to make a differential diagnosis of sarcomatoid cancers from true metastatic or primary sarcomas of the liver.

https://acsjournals.onlinelibrary.wiley.com/doi/pdf/10.1002/1097-0142%2819910701%2968%3A1%3C93%3A%3AAID-CNCR2820680119%3E3.0.CO%3B2-G

An immunohistochemical study of sarcomatoid liver carcinomas

The association of breast-cancer survival with various risk factors was investigated using data of 213 breast-cancer patients who underwent surgical operation between 1975 and 1978. They were followed-up until 1987, and a total of 64 deaths including 47 breast-cancer deaths were certified. The 5-year and 10-year relative survival rates were 78.5% and 75.3% respectively. Of the various factors investigated, some anthropometric indicators revealed interesting results; i. e., body weight, Quetelet index, and body surface area at the time of operation turned out to be strong predictors of survival with a statistically significant trend towards lower survival with larger body structure even after adjustment for confounding factors (e. g., clinical stage) using a proportionalhazard model. The estimated survival probability for women with Quetelet index of 20 was about 12% higher than that with Quetelet index of 24 over a 10-year or more follow-up period. Other variables exhibiting prognostic importance were clinical stage, TNM classification, and some histological findings, while height and reproductive life indicators were, as a rule, not significantly related to survival.

Akio Horie

Papers

Immunocytochemical markers of uncommon pancreatic tumors. Acinar cell carcinoma, pancreatoblastoma, and solid cystic (papillary-cystic) tumor.

Morphogenesis of pancreatoblastoma, infantile carcinoma of the pancreas. Report of two cases

Medullary arteries in aging and dementia.

An immunohistochemical study of sarcomatoid liver carcinomas

Survival of breast‐cancer patients and body size indicators