Capillary Fragility Research Articles

Capillary fragility and conjunctival vascular changes in relation to retinopathy in young diabetics.

Capillary fragility and conjunctival vascular changes in relation to retinopathy in young diabetics.

Relationship of platelet serotonin to disturbances of clotting and hemostasis.

The presence of serotonin (5-hydroxytryptamine) in high concentration in platelets and its absence from normal platelet-free plasma suggest the possibility that this vasoconstrictor substance may play a role in hemostatic mechanisms. Platelet serotonin content measured by a fluorometric method in 94 patients showed an average content of 0.22 µg./ml. blood. In none of the disease groups studied, including hypertension, was a significant alteration found in platelet serotonin. However, the administration of reserpine resulted in a marked and prolonged depletion of platelet serotonin that was not accompanied by any significant change in any of the clotting factors. The in vitro addition of serotonin in amounts up to 50 µg./ml. also failed to alter any of the clotting factors studied. Platelet serotonin did not correlate with diagnosis, age, weight, blood pressure, cephalin-fluocculation, or capillary fragility. However, markedly anemic patients (below 10 Gm. per cent hemoglobin) and patients whose blood urea nitrogen was above 30 mg. per cent, tended to have a low platelet serotonin content.

The vitamin C nutritional status and capillary fragility in chronic mental patients.

The vitamin C nutritional status and capillary fragility in chronic mental patients.

THE MANIFESTATIONS AND DIAGNOSIS OF BABESIA INFECTIONS

In spite of a considerable literature on the Babesia infections of animals, there are comparatively few references to atypical manifestations of the disease. The existing references are reviewed in this paper. They include cases manifested by ocular, respiratory, digestive, nervous, and rheumatic symptoms.Since the causal agents are not always demonstrable in smears of the peripheral blood, and since the disease picture can be so very variable, the criteria of diagnosis are laid down and discussed. A number of cases studied at the Onderstepoort Veterinary Institute, Onderstepoort, Union of South Africa, are described according to the body systems mainly involved. Respiratory symptoms include a range from simple catarrhs to intense dyspnea simulating pneumonia. A striking group is made up by the involvement of the circulatory system, presenting such symptoms as severe ascites, asymmetrical edemas, and purpuric lesions. In the nervous system, Babesia infections are represented in animals by the manifestation of epileptiform fits, aberrations of the gait, abnormal actions and postures, and peripheral nerve palsies. Enteritis and gastritis indicate involvement of the digestive system.The pathogenesis of the atypical lesions is discussed in considerable detail in the light of the pathological and clinicopathological changes that take place in the babesioses. These changes include blocking of the capillaries by agglomerations of parasitized red blood corpuscles with consequent local tissue anoxia and intoxication, anemia, hypoalbuminemia, degeneration of the liver and kidneys, capillary fragility, and marked coagulation defects of the blood.In all these changes and manifestations there is a close parallel with those encountered in malaria from time to time, particularly in the malignant tertian form. Important references from the literature of malaria are cited in support of this observation.

Palatine petechiae, an early sign in infectious mononucleosis.

• In 21 of 38 cases of proved and one case of probable infectious mononucleosis petechial eruption on the soft palate was observed. The eruption consisted of multiple pin-point lesions on the soft palate, usually near the junction with the hard palate but sometimes near the midline more posteriorly. In one patient the petechiae were also noted on the uvula. The number varied from 10 to several hundred. They appeared from 3 days to two weeks after the onset of symptoms, lasted from 3 to 11 days, and then faded, leaving no trace. In two cases in which platelet counts, capillary fragility tests, and clot retraction tests were done, there was no sign of a hemorrhagic diathesis. This eruption was primarily responsible for an early, correct diagnosis of infectious mononucleosis in two instances.

ACTH and cortisone therapy for recurrent massive gastric hemorrhage after subtotal gastrectomy; report of a case.

THE purpose of this report is to indicate the value of ACTH and cortisone in massive gastric bleeding due to capillary fragility associated with erosions of the gastric mucosa. This local capillary fragility may be converted to capillary resistance. The effectiveness of ACTH and cortisone in hemostasis has been described by several hematol-gists1 2 3 4 5 6 7 8 in treatment of thrombocytopenic purpura. Here, the improvement in bleeding time corresponded with the rise in capillary resistance and not with the change in the platelet count. Vascular Factors in Hemostasis The mechanism whereby ACTH affects hemostasis is indicated at least partly by Robson and Duthie,2 who . . .

Thrombocytopenic purpura due to quinidine.

Werlhof in 1735 was the first to describe a symptom complex of hemorrhagic purpura. The essential type of this disease is sometimes referred to as Werlhof's disease. Thrombocytopenic purpura is characterized by multiple hemorrhages into the skin and mucous membranes. One of the earliest indications of hemorrhage may be epistaxis, and the otolaryngologist may be the first to suspect the diagnosis and be instrumental in the institution of early treatment. Thrombocytopenic purpura is characterized by prolonged bleeding time, poor clot retraction, an increase in capillary fragility, and a decrease in circulating platelets. It may be classified as (1) the essential, or primary, type and (2) the symptomatic, or secondary, type. In 1946 Dameshek and Miller suggested that the essential type was due to a splenic factor acting to prevent the formation of platelets. The symptomatic type was found with hypoplastic bone marrow. This may be due to a nutritional

William Harvey and the pulmonary circulation.

Previous articleNext article No AccessWilliam Harvey and the Pulmonary CirculationDonald FlemingDonald Fleming Search for more articles by this author PDFPDF PLUS Add to favoritesDownload CitationTrack CitationsPermissionsReprints Share onFacebookTwitterLinkedInRedditEmail SectionsMoreDetailsFiguresReferencesCited by Isis Volume 46, Number 4Dec., 1955 Publication of the History of Science Society Article DOIhttps://doi.org/10.1086/348427 Views: 4Total views on this site Citations: 7Citations are reported from Crossref Copyright 1955 History of Science Society, Inc.PDF download Crossref reports the following articles citing this article:J. Alberto Neder Cardiovascular and pulmonary interactions: why Galen’s misconceptions proved clinically useful for 1,300 years, Advances in Physiology Education 44, no.22 (Jun 2020): 225–231.https://doi.org/10.1152/advan.00058.2020John B. West Fragility of pulmonary capillaries, Journal of Applied Physiology 115, no.11 (Jul 2013): 1–15.https://doi.org/10.1152/japplphysiol.00229.2013John S. White William Harvey and the primacy of the blood, Annals of Science 43, no.33 (Aug 2006): 239–255.https://doi.org/10.1080/00033798600200231Robert F. Grover, Wiltz W. Wagner, Ivan F. McMurtry, John T. Reeves Pulmonary Circulation, (Jan 2011): 103–136.https://doi.org/10.1002/cphy.cp020304Alfred P. Fishman, Dickinson W. Richards Air and Blood, (Jan 1982): 3–70.https://doi.org/10.1007/978-1-4614-7546-0_1ARNOLD M. KATZ Knowledge of the Circulation Before William Harvey, Circulation 15, no.55 (May 1957): 726–734.https://doi.org/10.1161/01.CIR.15.5.726 Conway Zirkle , John F. Fulton , I. E. Drabkin , Carl B. Boyer , I. Bernard Cohen , and Katharine Strelsky Eighty-First Critical Bibliography of The History of Science and Its Cultural Influences (To 1 January 1956), Isis 47, no.33 (Oct 2015): 247–360.https://doi.org/10.1086/348506

Management of the diabetic with vascular disease.

Vascular disease and its devastating end-results constitute one of the major problems faced by the medical profession today. The steadily increasing duration of life, with large numbers of the population living to sixty-five years of age and over, is bringing in an era in which degeneration of all systems must constitute a challenge. The diabetic too must pay the price of living longer by being more likely to develop degenerative disease and its complications. The remarkable contributions in the field of vascular disease during the last three decades have added to the insight into these disorders. It is commonly considered that involvement of the vascular system is inevitable in the diabetic, provided he lives long enough. One does see, however, a few individuals with diabetes of many years’ duration who seem to have escaped the ravages of time and have no demonstrable changes in their vascular tree. That arteriosclerosis in diabetes increases with the duration of the disease is evidenced by the figures quoted by Root, who noted that this process as a cause of death increased from 17 per cent at an average age of 44.5 to 70 per cent at an average age of 65.3. As will be discussed below, diabetics seem to have a greater incidence of arteriosclerosis and atherosclerosis than does the general population. Although these conditions appear to differ in no respect from those found in nondiabetics, nevertheless, there is evidence that certain vascular changes, particularly in the retina and kidneys, may well be peculiar to the complicated metabolic disturbance found in diabetes mellitus. In many organs of the diabetic, vascular lesions are found with special frequency. They will be more fully described as the individual anatomic units are discussed. White, who studied juvenile diabetics who had lived twenty years or more after developing the disease, noted some evidence of vascular disease in 92 per cent, an astounding figure. Factors playing a role in this increasing incidence, such as an inheritance of a defective vascular tree, seem to have some influence. Nutrition in a broad sense, infection (which is notoriously more frequent in the diabetic), so-called toxic factors, hormone imbalance, and capillary fragility all may play a part, although one cannot justifiably accuse any one of these.

Thrombocytopenic purpura in pregnancy.

Idiopathic thrombocytopenic purpura is a rare disease. The concomitant occurrence of this entity with pregnancy is an unusual finding and furthermore carries a high mortality. Yet such cases are truly worth extensive study and indeed have led to a significant clarification of the pathogenesis of thrombocytopenic purpura. Following is a report of a pregnant patient who had thrombocytopenic purpura. It will be followed by a discussion of some of the recent work on the pathogenesis of the platelet deficiency. The capillary fragility and the coagulation defect in this disease will not be discussed. REPORT OF A CASE A 27-year-old white housewife entered Colorado General Hospital for the first time on Feb. 23, 1954, with chief complaints of epistaxis, hematuria, and purpura of one month's duration and pregnancy of five months' duration. Social, personal, and family histories were noncontributory. History revealed that she had acute rheumatoid arthritis at age 12, involving

Blood-stream infection due to Proteus vulgaris and causing thrombocytopenic purpura; recovery with the use of chloramphenicol.

TWO thousand years ago purpura was recognized as a manifestation of pestilential fevers. Needless to say, since then the analysis of purpuric conditions has made great progress, and thrombocytopenia with purpura has been observed in many infectious states, such as septicemia, typhoid fever, typhus, relapsing fever, tuberculosis, small pox, chicken pox, vaccinia, scarlet fever, measles, rubella and subacute bacterial endocarditis.1 The degree of thrombocytopenia and increased capillary fragility associated with infectious conditions of apparently equal severity depends on the susceptibility of the patient's tissues rather than the intensity of the primary infection.2 The most likely cause of the thrombocytopenia, according . . .

Effect of roentgen irradiation and other types of injurious agents on capillaries.

SummaryBy means of a microinjection method it was possible to measure the fragility of mesenteric capillaries of the frog. Roentgen irradiation, heparin injection, trypsin and peptone shock increase the fragility of the capillaries. The increased capillary fragility appears to be a consequence of a liberation of heparin into the circulation of the animals, due to the irradiation or shock treatments.

Diabetic retinitis

SummaryIt is generally admitted that 30 % of diabetic patients show retinal changes. These are first venous microaneurysms. Later, haemorrhages and exsudates appear. These changes arc not thought to be specifically diabetic, although they are quite distinct from hypertensive changes. Nevertheless, most observ- ators correlate diabetic retinopathy with vascular changes shown in coronary, peripheral and renal vasculatures.We have not been able to find such a relation in our cases, except for renal lesions.Capillary fragility has been studied in some diabetic patients with retinopathy. Capillary fragility was increased in eight. This point should he reinvestigated in a larger group of diabetic patients.In some apparently normal individuals, routine ophthalmoscopy has shown diabetic retinal changes. All these patients show a decreased glucose tolerance curve.

Erythrophagocytosis and thrombocytopathy occurring during the course of a Henoch-Schönlein syndrome due to quinine

A patient is presented who exhibited a Henoch-Schönlein type of response after each of four administrations of quinine. At various times during these four episodes a number of typically immuno-hematologic disorders appeared: erythrophagocytosis, a serum factor that could induce erythrophagocytosis in normal blood, increased capillary fragility, transient diminution in numbers of platelets, abnormal platelet morphology, possible phagocytosis of platelets and decreased clot retraction. It is suggested that the occurrence of such immunohematologic phenomena, well known in other contexts to be due to specific antibody behavior, lends support to the contention that the Henoch-Schönlein syndrome is an example of antibody depredation upon tissues. The occurrence of erythrophagocytosis, induced by the activity of the patient's serum on normal blood, is especially strong associational evidence for this point of view.

Effect of Antihyaluronidase on the Capillary Fragility of the Diabetic

Effect of Antihyaluronidase on the Capillary Fragility of the Diabetic

Roentgenologic observations in hemorrhagic fever.

Hemorrhagic fever was first encountered by western physicians when it appeared among the United Nations Forces in Korea in 1951. Osaka Army Hospital served as a center for the treatment of this disease at that time. A comprehensive study of 300 observed cases with 9 deaths has been reported by one of us (1, 2). The purpose of this paper is to present the roentgenologic observations in hemorrhagic fever. To our knowledge, roentgenograms of patients with this disease have not previously been published in the literature. Reviews of the Japanese and Russian literature (3, 4, 5) revealed reports of 491 cases of hemorrhagic fever from Manchuria and 125 cases from eastern Siberia between the years 1932 and 1944. No cases were reported after 1944 until the disease broke out in Korea during 1951. In that year, 1,016 cases were recorded among the United Nations Forces (6). During early Manchurian outbreaks, the Japanese called the disease Songo fever and other names, according to the region of occurrence, but in 1942 they officially adopted the name epidemic hemorrhagic fever (5). The Russians, on the other hand, referred to the same disease in Siberia as endemic hemorrhagic nephroso-nephritis (3, 4). Although the Japanese and Russians (3, 4, 5) claimed to have furnished experimental proof that the disease is due to a filtrable virus, American workers, in spite of intense effort, have been unable to identify the causative agent (7). Clinical Course The incubation period in hemorrhagic fever varies from seven to as long as forty-six days, with an average of two to three weeks. The course follows a common clinical pattern consisting of three fairly well defined phases, which one of us (1, 2) has termed the invasion, toxic, and convalescent stages. The invasion stage usually lasts from two to five days and is characterized by an acute onset with high fever, accompanied mainly by symptoms and signs common to acute febrile illness and laboratory studies which are generally within normal limits. The toxic stage usually begins from the third to the fifth day and lasts until the tenth to the fourteenth day of illness. Shock is common early in this stage and is followed by renal failure. A hemorrhagic diathesis, evidence of cerebral toxicity, and gastrointestinal disturbances occur throughout this entire period. The most significant laboratory findings are albuminuria, oliguria and hyposthenuria; azotemia with hyperpotassemia; leukocytosis, often with leukemoid reaction and atypical lymphocytes ; hemoconcentration; rapid sedimentation rate; thrombocytopenia; prolonged bleeding time; and increased capillary fragility. The convalescent stage usually begins between the tenth and fourteenth day and lasts for as long as four months. Polyuria and hyposthenuria with inability to concentrate urine normally are the most prominent and persistent findings during this phase. Pathology The pathological aspects have been completely covered elsewhere (2).

Stress and Capillary Resistance (Capillary Fragility)

Stress and Capillary Resistance (Capillary Fragility)

Tests for so-called capillary fragility of the skin and the significance of positive tests in vascular disease

Positive capillary fragility or positive tourniquet tests are terms used loosely to describe intracutaneous hemorrhage produced by standardized doses of trauma (suction or venous compression). These tests for capillary fragility are crude and cannot be performed accurately by counting petechiae. Sources of error are numerous and can be overcome only by making numerous tests on different days. In the recorded results of this paper intracutaneous hemorrhage in the test is graded one to four plus. Inconstant and inconclusive results have been discarded. A higher incidence of positive tests is found in older patients. Patients with diabetes mellitus which coexisted with hypertension or other vascular disease showed an extremely high incidence of positive capillary fragility tests and this corresponds to the well known high incidence of spontaneous retinal and skin hemorrhages in such patients. All patients with hypertension and also those with arteriosclerotic disease without hypertension showed moderately high incidence of positive fragility tests.

Capillary fragility and menstruation: Salvatore, Carlos Alberto: Surg., Gynec. & Obst. 95: June, 1952

Capillary fragility and menstruation: Salvatore, Carlos Alberto: Surg., Gynec. & Obst. 95: June, 1952

Allergic purpura, including purpura due to foods, drugs and infections

1. 1. Purpura is due to a vascular lesion. Thrombocytopenia, when present, tends to increase the haemorrhagic tendency. 2. 2. Platelets and capillary endothelium are antigenically related. An antibody which injures the platelets can also damage the capillary endothelium. Thrombocytopenia and capillary endothelial damage may, therefore, have a common cause. 3. 3. Allergic purpura is of two types: (1) Purpura associated with an erythematous skin lesion, and also with joint and visceral symptoms: the Henoch-Schönlein syndrome. This syndrome is generally regarded as a manifestation of allergy but, apart from a very small proportion of cases which are undoubtedly due to hypersensitivity to foods, the cause of the syndrome is unknown and its allergic basis is entirely unproved. (2) True purpura in which the surrounding skin is normal. It may be due to an abnormal reaction to an infection or to a drug or, occasionally, to some other substance but is rarely if ever due to foods. Many infections and drugs can cause, in different individuals, both thrombocytopenic and athrombocytopenic purpura. 4. 4. Cases of true purpura due to infections may be divided into those which occur at the height of an infection and those which occur during convalescence. The former type appears to be due to an abnormal susceptibility of the patient's tissues to the factors which normally cause thrombocytopenia and increased capillary fragility at the height of an infection. If this abnormal susceptibility is shown only by the vascular endothelium, athrombocytopenic purpura will result. If the megakaryocytes and platelets are also affected, the purpura will be thrombocytopenic. Purpura occurring during convalescence can best be explained on the assumption of an allergic basis, similar perhaps to that to which nephritis following streptococcal infections has been attributed. 5. 5. The only example of purpura due to a drug which has been subjected to experimental analysis is thrombocytopenic purpura due to sedormid (allyl-isopropyl-acetyl-carbamide). Sedormid appears to act by combining with platelets, so conferring upon them the properties of a weak antigen. This antigen is formed whenever the drug is taken but it has the power of stimulating antibody formation in only a very small proportion of those taking the drug. Thrombocytopenia occurs only in those who develop the antibody and is due to lysis of the platelet-sedormid antigen by antibody and complement. The capillary lesion is probably produced in a similar way, the drug combining with the endothelial cells to form a further antigen which then reacts with the antibody which causes platelet lysis, this reaction producing the vascular lesion which plays such an important part in the development of purpura. It is not known how far these findings are applicable to purpura due to other drugs. An isolated observation on thrombocytopenic purpura due to quinine suggests that the mechanisms underlying sedormid purpura may be similar to those underlying thrombocytopenic purpura due to other drugs. In athrombocytopenic purpura due to drugs it is suggested that only the capillary endothelium combines with the drug to form an antigen, and therefore that it alone reacts with the antibody, this reaction causing the capillary lesion.