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Critically ill patients should be susceptible to pulmonary thromboembolism (PTE). To determine the incidence of acute PTE in this patient population, we reviewed hospital charts and autopsy findings of all Class IV critically ill patients admitted to our hospital's Recovery Room-Acute Care Unit, between 1972 and 1982. Massive PTE either contributed to or was the sole cause of death in only two of the 152 patients studied (1.3%). Small single or scattered PTE were an incidental finding not contributing to morbidity or mortality in 13 patients. No gross evidence of PTE was found in the remaining 137 patients. There was no relationship between the occurrence of PTE and obesity, polycythemia, platelet count, PT or PTT, ventilatory support, level of PEEP, fluid balance, intravascular catheter days, pulmonary artery pressure, or pulmonary vascular resistance. Twelve patients did not have PTE at autopsy though it was seriously considered during ICU management. Unlike many other types of hospitalized patients, Class IV critically ill surgical patients are highly unlikely to suffer from PTE. When acute cardiorespiratory decompensation occurs, other more common causes should be given primary consideration.
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PMID:The autopsy incidence of acute pulmonary embolism in critically ill surgical patients. 379 56

All contributory factors to the unusual occurrence of stroke in young people were evaluated in patients under age 40 admitted to the Stroke Unit of the Austin Hospital in Melbourne, Australia. Over the August 1977 to December 1980 period there were 700 admissions. Of these 14 patients were under the age of 40. There were 7 males and 7 females whose ages ranged from 17-38 years. Each patient was screened for factors which might contribute to premature vascular disease including hypertension, diabetes, smoking, obesity, and hyperlipidemia. In addition, the following tests were performed to exclude an arteritic process: full blood examination; ESR; protein electrophoresis; syphilis serology; and the presence of antinuclear factor. Each of the 14 patients suffered cerebral infarction. A summary of each case is presented in a table. In 9 patients, infarction occurred in the carotid territory of supply. Large cortical infarcts with or without subcortical involvement occurred in cases 1-8, of whom 5 had major vessel occlusion demonstrated angiographically and another had stenosing and ulcerative atheromatous disease at the extracranial carotid bifurcation. In a further 4 patients, infarction occurred within the vertebrobasilar territory and was either confined to the brain stem, the occiptal cortex, or involved both. Angiograms were performed in 2 of these patients and showed irregular narrowing of the vertebral artery which was interpreted as spasm and segmentally narrowing of the basilar artery. The final patient had several ischemic events which included right sided amaurosis fugax, and left frontal, right parieto-occipital and left occipital infarctions. Angiography was normal. All patients survived the stroke and were able to go home. There may be an interrelationship between the pathological findings of Irey et al. (1978) and the effect oral contraceptives (OCs) has on migraine. This is relevant to Case 13. Sustained exposure to OCs may produce the pathological changes described (visible as segmental narrowing angiographically). In 2 patients cerebral infarction was caused by atheromatous or hypertensive occlusive vascular disease. In Case 3 an embolus occluded the middle cerebral artery. Infarction complicating migraine was diagnosed confidently in 4 patients on the basis of typical migrainous symptomatology in the past and accompanying the stroke. Of the 12 patients fully evaluated, there were no cases of polycythemia or thrombocytosis. There were no abnormalities of the clotting factors. Almost every patient had some form of emotional upset, and there were 7 who had significant psychiatric illness and emotional problems of extreme magnitide.
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PMID:Stroke syndromes in young people. 692 82

The diffusing capacity for carbon monoxide is partially dependent on lung volume at which it is measured. As a consequence, the diffusing capacity for carbon monoxide is often indexed to the simultaneously measured lung volume (VA), giving rise to the term DL/VA. This reflects the diffusing capacity of carbon monoxide per unit area of lung parenchyma. The authors investigated the pulmonary function of 18 patients who had an elevated DL/VA in order to identify factors that could account for this abnormality. Sixteen of the 18 had a reduction in vital capacity. The vital capacity was reduced because of obesity, pleural disease, and diaphragmatic dysfunction. Eight of nine patients with a body mass index > 30 kg/m2 had a reduction in vital capacity. On the basis of these findings, we believe that an elevated DL/VA should alert the physician to the possibility of 1) an increase in pulmonary capillary blood volume (Vc) (obesity, polycythemia, negative pleural pressure), and 2) reduced VA that does not directly affect the pulmonary capillary bed (pleural disease, neuromuscular disease).
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PMID:Clinical correlates of an elevated diffusing capacity for carbon monoxide corrected for alveolar volume. 865 53

The perinatal mortality rate of infants of diabetic mothers (IDMs) has declined dramatically from 250 per 1000 live births in the 1960s to a near-normal 20 per 1000 live births in the 1980s. Five to 8% of all IDMs suffer from major congenital malformations, and it is the latter that are responsible for 50% of these perinatal deaths. It has been shown that tight glycemic control prior to conception and during pregnancy can prevent an excess rate of congenital malformations, fetal macrosomia, birth trauma, and neonatal respiratory distress syndrome. We briefly review the short- and long-range complications that occur in offspring of diabetic mothers (ODMs) from gestation through young adulthood. Short-term neonatal complications, such as hypoglycemia, hypocalcemia, hypomagnesemia, hyperbilirubinemia, and polycythemia, are related mainly to fetal hyperinsulinemia, hypoxemia, and prematurity. They are readily controllable within the setup of modern neonatal intensive care units. Long-range complications include an increased rate of childhood and adolescent obesity, impaired glucose tolerance or diabetes mellitus, and subtle neuropsychological dysfunctions. These may be related to the severity of the maternal hyperglycemia during pregnancy, the consequent fetal hyperinsulinemia, and third trimester maternal lipid metabolism disturbances. Today we have at hand the knowledge and tools to properly treat both pregestational and gestational diabetes. Increased education of the general practitioner and the target population regarding early referral of pregestational diabetic mothers and the implementation of screening programs for gestational diabetes will further reduce diabetic pregnancy-related morbidity.
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PMID:Short- and long-range complications in offspring of diabetic mothers. 888 19

A fifty-one-year-old man presented with a history, symptoms, and clinical findings typical of a hypothenar hammer syndrome in his dominant hand. A thrombotic obstruction in the distal section of the ulnar artery with multiple downstream occlusions of proper digital arteries were documented angiographically. Coexistence of additional cardiovascular risk factors (smoking-induced polycythemia, obesity, hypercholesterolemia, and hypertension) was identified. Conservative management with intravenous heparin and prostaglandin E1 together with measures directed at controlling the additional risk factors (repeated venesection, immediate smoking cessation, and low-lipid diet) resulted in a striking clinical and angiographic improvement of the digital perfusion, without resort to interventional measures or thrombolysis.
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PMID:Hypothenar hammer syndrome successfully managed with intravenous prostaglandin E1 and heparin and with correction of the thrombogenic risk profile. A case report. 892 62

A 32-year-old, hypertensive, morbidly obese (BMI 49 kg/m2) woman was referred to us suspected of sleep-disordered breathing. Polycythaemia, right heart and respiratory failure, restrictive ventilatory impairment, decreased hypercapnic respiratory drive, high number of very short apneas mostly of central origin (698 vs 530 obstructive), and overnight hypoxaemia were found. The diagnosis of obesity-hypoventilation syndrome was established and the treatment with almitrine, aminophylline and low-calorie diet was started. After 6 months body weight decreased significantly (BMI 38 kg/m2). RBC, spirometry, blood gas analysis, overnight oximetry, hypercapnic respiratory drive and polysomnography showed results within normal limits. Causes, pathophysiology and possible treatment of obesity-hypoventilation syndrome are discussed.
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PMID:[Obesity and hypoventilation syndrome; effects of weight loss and treatment with respiratory stimulants]. 899 66

The introduction of new immunosuppressive regimens results in the significant improvement in the outcome of patients after kidney transplantation. However, about 5 percent of renal transplants are lost every year. Not only immunological (alloantigendependent) but also nonimmunological (alloantigen-independent) factors are involved in late graft loss. Among them, hypertension, hyperlipidemia, proteinuria, genetic predisposition, viral infection and nephrotoxicity of immunosuppressive drugs contribute to the development and to the progression of chronic post-transplant nephropathy. Hypertension can be both the cause and the consequence of chronic allograft failure. Hypertension is frequently observed before transplantation, persists after grafting and increases the risk of chronic allograft nephropathy. Hypercholesterolemia, obesity, atheromatosis, polycythemia, and excessive salt intake are factors contributing in post-transplant hypertension. However, in some cases, hypertension can be transferred with the grafted kidney, as observed in normotensive patients before renal transplantation. In 1 to 12 percent of cases, the cause of post transplant hypertension is the stenosis of the transplant artery. Sometimes the presence of hypertension in renal recipients may result from the recurrence of glomerulonephritis or from the development of glomerulonephritis de novo in the graft. Also immunosuppressive treatment with corticosteroids and cyclosporine A contributes to the increased prevalence of hypertension by 20-30 percent. The development of the graft nephroarteriolosclerosis as a consequence of hypertension accelerates the progression of the post-transplant nephropathy. Adequate control of the arterial pressure (< 140/90) should be achieved in all renal transplant recipients. Reduction in protein and salt intake is important to reduce hyper-filtration and slows the progression of transplant nephropathy. However, pharmacological treatment is usually needed. Angiotensin-converting-enzyme inhibitors, angiotensin II type I receptor antagonists exhibit beneficial hemodynamic effect leading to the reduction of glomerular hypertension and proteinuria. Calcium antagonists besides their systemic antihypertensive effect, can protect renal grafts from vascular and renal toxicity of CyA. Sometimes, combined therapy with these and other antihypertensive drugs and diuretics is necessary.
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PMID:[Post-transplant nephropathy and arterial hypertension]. 1186 48

Cystic renal lymphangiectasia (CRL) is a rare malformation of lymphatics that can present in childhood and adulthood. Symptoms and radiologic features are relatively well defined, but clinical evolution and prognosis remain unclear. We treated a boy with CRL who developed chronic renal insufficiency. The first manifestation was abdominal swelling associated with an umbilical hernia noted incidentally at 1.6 years. Computed tomography with intravenous contrast administration demonstrated perirenal cysts with fluid collection, suggesting CRL. Intractable ascites resisted pharmacologic treatments such as diuretics. After approximately 7 years, the ascites resolved spontaneously, but the perirenal cysts persisted. At 11 years, proteinuria was noted. A renal biopsy specimen showed interstitial abnormalities consistent with CRL, glomeruli showed a focal segmental mesangial increase. Proteinuria persisted despite administration of an angiotensin-converting enzyme inhibitor, increasing as obesity and hypertension worsened. Renal function gradually declined in the ensuing years. Polycythemia coexisted with a normal serum erythropoietin concentration. A follow-up renal biopsy specimen disclosed glomerular enlargement together with focal segmental mesangial expansion, suggesting obesity-related glomerulopathy. Our observation suggest that under some specific circumstances like our patient CRL may exacerbate. Management of complicating obesity and hypertension are likely to be important for maintaining normal renal function, especially in the diffuse bilateral type of CRL present in our patient.
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PMID:Chronic renal insufficiency in a boy with cystic renal lymphangiectasia: morphological findings and long-term follow-up. 1818 26

We here report a case of a 53-year-old woman requiring pulmonary embolectomy for acute massive pulmonary embolism caused by a huge uterine myoma compressing veins in the pelvis and extreme obesity. She was also diagnosed as having myomatous erythrocytosis syndrome, a rare disease associated with secondary polycythemia. The polycythemia improved after a hysterectomy which was performed after pulmonary embolectomy.
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PMID:Pulmonary embolism with myomatous erythrocytosis syndrome and extreme obesity. 1962 99

Recently, the development of selective androgen receptor modulators (SARMs) has been suggested as a means of combating the deleterious catabolic effects of hypogonadism, especially in skeletal muscle and bone, without inducing the undesirable androgenic effects (e.g., prostate enlargement and polycythemia) associated with testosterone administration. 17beta-Hydroxyestra-4,9,11-trien-3-one (trenbolone; 17beta-TBOH), a synthetic analog of testosterone, may be capable of inducing SARM-like effects as it binds to androgen receptors (ARs) with approximately three times the affinity of testosterone and has been shown to augment skeletal muscle mass and bone growth and reduce adiposity in a variety of mammalian species. In addition to its direct actions through ARs, 17beta-TBOH may also exert anabolic effects by altering the action of endogenous growth factors or inhibiting the action of glucocorticoids. Compared to testosterone, 17beta-TBOH appears to induce less growth in androgen-sensitive organs which highly express the 5alpha reductase enzyme (e.g., prostate tissue and accessory sex organs). The reduced androgenic effects result from the fact that 17beta-TBOH is metabolized to less potent androgens in vivo; while testosterone undergoes tissue-specific biotransformation to more potent steroids, dihydrotestosterone and 17beta-estradiol, via the 5alpha-reductase and aromatase enzymes, respectively. Thus the metabolism of 17beta-TBOH provides a basis for future research evaluating its safety and efficacy as a means of combating muscle and bone wasting conditions, obesity, and/or androgen insensitivity syndromes in humans, similar to that of other SARMs which are currently in development.
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PMID:Tissue selectivity and potential clinical applications of trenbolone (17beta-hydroxyestra-4,9,11-trien-3-one): A potent anabolic steroid with reduced androgenic and estrogenic activity. 2013 77


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