Shock-like Reaction Research Articles

MRSA – global threat and personal disaster: patients' experiences

To ascertain and describe the patients' knowledge, perceptions and experiences of being methicillin-resistant Staphylococcus aureus (MRSA) positive. Antibiotic resistant bacteria are a serious global threat. MRSA can cause wound infection, pneumonia, septicaemia and mortality. This qualitative study has focused on patients' experiences of living with MRSA. Fifteen patients with MRSA-infected wounds were interviewed. All data were transcribed verbatim and analysed according to content analysis. Information about the MRSA diagnosis often caused a shock-like reaction. Patients' perception of being MRSA positive was stigmatizing as plague or leprosy; they felt dirty and felt that they were a severe threat to their environment. Fears of infecting someone else and being rejected were commonly expressed. The key findings emerged as a theme: Being exposed to others' shortcomings and being a threat to others' health. Three categories were identified: understanding and emotional reactions, treatment by the healthcare professionals and consequences and expectations. Gaps in both patient and staff knowledge of MRSA led to unnecessary misunderstandings, causing fear, social isolation and suffering. Living with MRSA can be extremely stressful for the patients. Knowledge and empathy from staff involved in their care is crucial to optimize patients' experiences. Staff education to meet patients' demand for information and prevent contamination is essential.

Feline heartworm disease: a clinical review.

Feline heartworm disease is caused by the filarial nematode Dirofilaria immitis, and is transmitted by mosquitoes in heartworm-endemic areas worldwide. While dogs are the definitive hosts for this parasite, cats can also be infected, and the overall prevalence in cats is between 5% and 10% of that in dogs in any given area. The spectrum of feline presentations varies from asymptomatic infections to chronic respiratory signs, sometimes accompanied by chronic vomiting to acute death with no premonitory signs. Ante-mortem diagnosis can be challenging and relies on a combination of tests, including antigen and antibody serology, thoracic radiography and echocardiography. As treatment with heartworm adulticidal drugs can be life-threatening and heartworm infection in cats is often self-limiting, infected cats are frequently managed with supportive treatment (corticosteroids, bronchodilators, and anti-emetics). Surgical removal of filariae using extraction devices may be considered in some acute cases where immediate curative treatment is necessary, but filarial breakage during the procedure may result in an acute fatal shock-like reaction. Necropsy findings are mainly pulmonary and include muscular hypertrophy of the pulmonary arteries and arterioles on histopathology. A number of safe and effective macrocytic lactone drugs are available for prophylaxis in cats. These drugs can kill a range of larval and adult life-cycle stage heartworms, which may be advantageous in cases of owner compliance failure or when heartworm infection status is undetermined at the time prophylaxis is commenced. An index of suspicion for feline heartworm disease is warranted in unprotected cats with respiratory signs, and perhaps chronic vomiting, in areas where canine heartworm disease is endemic. Many cats, once diagnosed and with appropriate supportive care and monitoring, will resolve their infection and be free of clinical signs.

IL‐10 is not required to prevent immune hyperactivity during memory responses to Toxoplasma gondii

Primary infection of IL-10 knockout (KO) mice with the protozoan parasite Toxoplasma gondii leads to a CD4(+)-T-cell dependent shock-like reaction with high systemic levels of IL-12 and IFN-gamma, severe liver pathology and death of mice. In the present study, this immune-mediated pathology was prevented by treatment of IL-10 KO mice with the anti-parasitic drug sulfadiazine, allowing these mice to progress to the chronic phase of infection. To address the role of endogenous IL-10 in the regulation of secondary immune responses to T. gondii, IL-10 KO mice were infected with the avirulent Me49 strain of this parasite, treated with sulfadiazine for 2 weeks starting at day 3 p.i., and were rechallenged 6 weeks p.i. with RH, a highly virulent strain of T. gondii. In these studies, chronically infected IL-10 KO mice survived secondary infection with RH and controlled parasite load. Although serum levels of IL-12 and IFN-gamma were higher in IL-10 KO mice than in wild type (WT) mice 8 days after RH rechallenge, these levels were well controlled in the absence of endogenous IL-10, suggesting that IL-10 is not required to down-regulate cytokine production during the memory response. Antigen-specific ex vivo recall responses further revealed that splenocytes from chronically infected WT and IL-10 KO mice responded to parasite antigen with similar production of IL-12 and IFN-gamma, and there was also no significant difference in ex vivo production of these cytokines by splenocytes in response to parasite antigen 7 days after secondary infection with T. gondii. Furthermore, IL-10 KO mice immunized with the Ts-4 vaccine-strain of T. gondii were protected when rechallenged with the virulent RH strain. Together, these studies demonstrate that the inhibitory effect of IL-10, which is required to prevent immune-mediated pathology during primary infection, is not required to prevent immune hyperactivity during a secondary response to T. gondii, and a highly effective memory response is generated in the absence of endogenous IL-10.

Contribution of Interleukin-12 (IL-12) and the CD28/B7 and CD40/CD40 Ligand Pathways to the Development of a Pathological T-Cell Response in IL-10-Deficient Mice

The ability of interleukin-10 (IL-10) to suppress accessory cell functions required for optimal T-cell activation makes it an important inhibitor of cell-mediated immunity. Thus, after infection with the protozoan parasite Toxoplasma gondii, IL-10 knockout (KO) mice develop a CD4(+)-T-cell-dependent shock-like reaction with high levels of IL-12 and gamma interferon (IFN-gamma) in serum, leading to death of mice during the acute phase of infection. Previous studies from this laboratory have shown that simultaneous blockade of CD28 and CD40 can prevent this lethal reaction by inhibiting the production of IFN-gamma. However, the blockade of costimulation did not affect systemic levels of IL-12. To better understand the relationship between IL-12 and the CD28 and CD40 pathways in mediating immune hyperactivity, antagonists of these factors were used to determine their effects on the development of a pathological T-cell response in IL-10 KO mice. Blockade of IL-12 or the CD28/B7 interaction alone did not affect survival; however, the combined blockade of both pathways resulted in decreased production of IFN-gamma and the survival of IL-10 KO mice. To assess the role of the two ligands for CD28, B7.1 and B7.2, IL-10 KO mice were treated with alphaIL-12 plus alphaB7.1 or alphaB7.2 or the combination of all three antibodies. These studies revealed that blockade of both B7 molecules is required for decreased production of IFN-gamma and survival of infected IL-10 KO mice, suggesting that B7.1 and B7.2 can contribute to the lethal shock-like reaction in IL-10 KO mice. In contrast, neutralization of IL-12 and blockade of the CD40/CD40 ligand (CD40L) interaction in vivo did not alter the production of IFN-gamma and only resulted in a small delay in time to death of mice. Together, these data suggest that the CD28/B7 interaction has a central role in the development of a pathological T-cell response in IL-10 KO mice, which is distinct from the role of the CD40/CD40L and IL-12 pathways.

Blockade of costimulation prevents infection-induced immunopathology in interleukin-10-deficient mice.

Interleukin-10 (IL-10) is associated with inhibition of cell-mediated immunity and downregulation of the expression of costimulatory molecules required for T-cell activation. When IL-10-deficient (IL-10KO) mice are infected with Toxoplasma gondii, they succumb to a T-cell-mediated shock-like reaction characterized by the overproduction of IL-12 and gamma interferon (IFN-gamma) associated with widespread necrosis of the liver. Since costimulation is critical for T-cell activation, we investigated the role of the CD28-B7 and CD40-CD40 ligand (CD40L) interactions in this infection-induced immunopathology. Our studies show that infection of mice with T. gondii resulted in increased expression of B7 and CD40 that was similar in wild-type and IL-10KO mice. In vivo blockade of the CD28-B7 or CD40-CD40L interactions following infection of IL-10KO mice with T. gondii did not affect serum levels of IFN-gamma or IL-12, nor did it prevent death in these mice. However, when both pathways were blocked, the IL-10KO mice survived the acute phase of infection and had reduced serum levels of IFN-gamma and alanine transaminase as well as decreased expression of inducible nitric oxide synthase in the liver and spleen. Analysis of parasite-specific recall responses from infected IL-10KO mice revealed that blockade of the CD40-CD40L interaction had minimal effects on cytokine production, whereas blockade of the CD28-B7 interaction resulted in decreased production of IFN-gamma but not IL-12. Further reduction of IFN-gamma production was observed when both costimulatory pathways were blocked. Together, these results demonstrate that the CD28-B7 and CD40-CD40L interactions are involved in the development of infection-induced immunopathology in the absence of IL-10.

Tumor necrosis factor-α release during systemic reaction in cold urticaria

Primary cold urticaria (PCU) characterized by the association of urticaria, angioedema, and sometimes a shock-like reaction after cold exposure, is usually considered to be linked with histamine and prostaglandin D 2 release by mast cells. To determine the involvement of cytokines, we studied the release of tumor necrosis factor-α (TNF-α) in the blood of the efferent vein after immersion of the hand in chilled water. Five patients with PCU were compared with a control population (three patients with nonphysical urticaria and three healthy subjects). Among patients with PCU who underwent the cold immersion test, two exhibited a shock-like reaction with a large urticarial plaque (patients 1 and 2), one had only a mild cutaneous reaction, and two had no reaction. Patient 1 was reevaluated after 6 months of treatment with H 1 and H 2 antihistamines: he did not respond to this challenge. All controls were strictly negative. Histamine was released within the first minute after the challenge in the three patients with PCU, but at a higher level for the two patients who had a systemic reaction. TNF-α was undetectable in the blood of the patient with only a mild cutaneous reaction, whereas TNF-α release was observed for the two patients with a systemic reaction, 2 and 6 minutes after the end of the cold immersion test. The two other patients and the control subjects released neither histamine nor TNF-α. In parallel, pathologic and immunohistochemical (with a rabbit anti-TNF-α antibody) studies were performed on skin biopsy specimens collected 10 minutes after ice-cube test. Four patients with PCU who had positive ice-cube test results were studied, as well as patient 1 after treatment, who did not respond to the ice-cube test. The pathologic study revealed that mast cells were the only cells infiltrating the dermis in PCU and that most of mast cells were degranulated but only in the four patients with positive ice-cube test results. Immunohistochemical study revealed that only mast cells were stained by anti-TNF antibody (90% ± 2.5%). In conclusion, besides histamine release, cold exposure in PCU induces a concomittent TNF-α release by mast cells. Its detection in blood suggests that in addition to histamine, TNF-α may be implicated in the shock-like reaction in cold urticaria.

Heartworm migration toward right atrium following artificial pulmonary arterial emobolism or injection of heartworm body fluid.

Heartworms harboring in the pulmonary arteries migrated toward the right atrium following insertion of dead heartworms or heartworm-like silicone tubes, or intravenous injection of body fluid extract of a female heartworm. The migration occurred within 3 hr (early group) or 1 to 7 days (late group) after insertion of dead worms, 1 to 11 days after insertion of silicone tubes, and immediately after infusion of heartworm-body fluid. The cardiac output decreased to an unmeasurably low level, and the pulmonary arterial pressure was also reduced in the early group. Although the output decreased, the pulmonary arterial pressure and the total pulmonary resistance increased gradually in the late group. In dogs with heartworm migration, in which silicone tubes had been inserted, the changes in cardiopulmonary values were the same as those in dogs of the late group. In dogs to which the body fluid had been administered intravenously, the changes in cardiopulmonary values were well accord with those in the early group. The systemic blood pressure also fell immediately after the administration with the shock-like state. These results suggest that the death of a part of the heartworms may be closely associated with the migration of heartworms toward the right atrium through the pulmonary arterial embolism and/or shock-like reaction by heartworm body fluid.

Prevention of adverse reactions following milbemycin D administration to microfilaremic dogs infected with Dirofilaria immitis.

Some adverse reactions such as shock-like reaction and dirofilarial hemoglobinuria (caval syndrome) occasionally occurred in microfilaremic dogs following milbemycin D (Milbe) administration. This study was carried out to seek the prevention of these adverse reactions. In two groups containing 16 and 9 dogs respectively which were administered either chlorpheniramine maleate (1 mg/kg) or indomethacin (2.5 mg/kg) simultaneously with Milbe (1 mg/kg), the incidence of clinical signs such as the pale color of the visible mucous membranes, respiratory disorders, caval syndrome and shock-like reaction as well as changes in clinical parameters such as RBC and WBC counts, WBC profile and serum total protein, were almost equal to that observed in the group administered Milbe alone. In 41 dogs administered prednisolone (1 mg/kg) simultaneously with Milbe (1 mg/kg), no shock-like reaction was observed. Changes in clinical parameters were different from those in the group administered Milbe alone, whereas some clinical signs of adverse reactions, including caval syndrome, were observed. These results indicated that prednisolone was effective for prevention of the shock-like reaction in microfilaremic dogs induced by Milbe.

犬糸状虫ミクロフィラリア寄生犬にイベルメクチンとジエチルカルバマジンを投与してみられる副作用の比較

The present study was designed to find out whether administration of ivermectin (IVM) to microfilaremic dogs causes the shock-like reaction that is well known as an adverse effect of diethylcarbamazine (DEC). Both IVM and DEC were given to the same dogs, and the occurrence of adverse reaction was compared between the two drugs. Thirty dogs, which had an average microfilaria count of 395 (11-3, 309)/20μl of peripheral blood, were used for the experiment. A single oral administration of IVM was given to each of the 30 dogs at the dose of 10μg/kg, and observation was continued for the following 7 days. In this period, there appeared no abnormality in clinical signs, WBC count, or in any of 13 items ofplasma biochemical test. There was no reduction in microfilaria count either after the administration. The DEC experiment was carried out after the IVM experiment was completed. A single oral administration of DEC-citrate was given to each of the 30 dogs at the dose of 6mg/kg. For the following 24 hours, the animals were observed for the appearance of clinical signs, and examined with the same test protocol as in the IVM experiment. Five dogs (16.7%) were judged to have suffered the shock-like reaction from one to three hours after the administration of DEC. In these dogs, the clinical signs were accompanied by an increase in WBC and marked rises in GOT, GPT and ALP, which indicated severe hepatic impairment. Even in the other 25 dogs that showed no clinical signs, similar changes were observed in the WBC and the biochemical test values, although the changes were milder.Thus, no abnormality associated with IVM administration was observed, even in the dogs that showed theDEC-associated shock-like reaction. Therefore, it appears that IVM has no tendency to cause the shock-like reaction which can occur following DEC administration in microfilaremic dogs.

Leukotriene C 4 metabolism by hepatoma cells and liver

The metabolism of the glutathionyl leukotriene LTC 4 in the mercapturic acid pathway was studied in suspensions of AS-30D hepatoma cells and hepatocytes, as well as in vivo in the bile duct-cannulated rat and in primates. 1. 1.|Isolated hepatocytes actively took up cysteinyl leukotrienes and metabolized LTC 4 not only to LTD 4 and LTE 4 but also to N-acetyl-LTE 4 and to metabolites more polar than LTC 4. 2. 2.|AS-30D hepatoma cells are deficient in the transport system for the uptake of cysteinyl leukotrienes. Peptide cleavage of LTC 4 to LTD 4 and LTE 4 was catalyzed by ectoenzymes of these cells. Inactivation of γ-glutamyl-transferase by acivicin and inhibition of LTD 4 dipeptidase by penicillamine largely prevented further catabolism of LTC 4 and LTD 4, respectively. 3. 3.|[ 3H]LTC 4 injected i.v. into rats was rapidly eliminated from the circulating blood, taken up by the liver, and excreted into bile where 77% of the administered radioactivity was recovered within 1 hr. The biliary LTC 4 metabolites included LTD 4, N-acetyl-LTE 4, and metabolites more polar than LTC 4. 4. 4.|Inhibition of [ 3H]LTC 4 metabolism in vivo by i.v. penicillamine shifted the pattern of biliary cysteinyl leukotrienes; an extended half-life of [ 3H]LTD 4 was associated with a retarded formation of N-acetyl-LTE 4 and of polar metabolites. 5. 5.|Endogenous cysteinyl leukotrienes elicited by trauma were measured after HPLC separation by radioimmunologic analysis in plasma and bile of rats. The biliary concentration of these leukotrienes was up to 100 times as great as in plasma. N-Acetyl-LTE 4 was the predominant endogenous metabolite in rat bile. 6. 6.|In the monkey Macaca fascicularis, cysteinyl leukotrienes were predominantly eliminated from blood via the liver into bile; renal excretion amounted to about 50% of the hepatobiliary elimination. Absorption of cysteinyl leukotrienes from the intestine resulted in enterohepatic circulation of these mediators. 7. 7.|Metabolites of [ 3H]LTE 4 injected i.v. in the monkey were analyzed in bile and urine. In addition to polar metabolites and a small percentage of [ 3H]LTD 4, [ 3H]LTE 4 was a predominant metabolite particularly in bile. LTE 4 was also the major endogenous cysteinyl leukotriene detected by radioimmunologic analysis in monkey bile. 8. 8.|LTE 4 was the predominant endogenous cysteinyl leukotriene measured in human bile in patients suffering from acute pancreatitis. The detected amounts of LTE 4 may be sufficient to induce known phenomena associated with acute pancreatitis including the shock-like reaction.

Clinical application of milbemycin D as a prophylactic agent against Dirofilaria immitis infection in dogs: reactions in uninfected and infected dogs.

A dose of 1mg/kg or 5mg/kg of milbemycin D, a new prophylactic agent for Dirofilaria immitis (heartworm), was given to 201 dogs orally and the reaction was investigated by symptomatic, hematological and biochemical examinations. Dogs were divided into 3 groups: uninfected by heartworm (uninfected group), infected without circulating microfilaria (mf negative group), and infected with circulating mf (mf positive group). The incidence and degree of clinical signs were not clearly different with either dose. Vomiting and arrhythmia, which were noted to show about the same incidence in 3 groups, were seen in a total of 5 (2%) and 22 (11%) dogs, respectively. Body temperature and blood pressure fell slightly, and RBC count, serum total protein concentration, osmolality and sodium concentration were also slightly decreased 3 and/or 6 hr after administration in the uninfected and mf negative groups. Almost all of these changes remained within the normal ranges, and tended to recover 24 hr after administration. No other reactions were seen in the uninfected group. Loss of appetite, pale visible mucous membranes, shock-like reaction and dirofilarial hemoglobinuria (caval syndrome) were noted in a total of 5 (2%), 9 (5%), 9 (5%) and 8 (4%) dogs, respectively, which were seen mainly in the mf positive group. A significant decrease of circulating mf count, rise in body temperature, serum GOT, GPT and ALP activities were also observed 24 hr after administration in the mf positive group. Shock-like reaction was seen in a dog of the mf negative group, but in this case a small number of microfilariae were detected in the liver and lungs on histopathological examination. The effects of dead mf might be involved in the reaction of the mf positive group. From these results, it is considered that clinical application of milbemycin D for uninfected and mf negative dogs presents no risks, but adverse reactions may occur in dogs with microfilaremia.

Heroin Pulmonary Edema

To the Editor: In the August, 1972 Clinical Pathologic Conference concerning heroin pulmonary edema, the statement is made … “since heroin induced pulmonary edema occurs only when there has been an overdose, hypersensitivity to heroin is an unlikely explanation for the cause of this syndrome.” Although overdose is the generally accepted initiating factor for many cases of heroin pulmonary edema, not all cases can be explained on this basis. Helpern writes … “in some acute fatal cases, the rapidity and type of reaction do not suggest simple overdosage, but rather an overwhelming shock-like reaction due to hypersensitivity to the injected material. The toxicologic examination of the tissues in such fatalities … demonstrated only the presence of the alkaloid and not overdosage.” Also, “unexpected acute deaths may occur in some addicts who inject themselves with heroin mixtures even though others who take the same usual aliquot dose from the same sample at the same time may suffer no dangerous effect.”1Helpern M Yong-Myun R Deaths from narcotism in New York City.Incidence, circumstance and postmortem findings. NY J Med. 1966; (Sept 16): 2391-2408Google Scholar, 2Helpern M Fatalities from narcotic addiction in New York City.Incidence, circumstances and pathologic findings. 1972; (Human Path 3: March)Google Scholar Fulton3Cherubin CE The medical sequelae of narcotic addiction.Ann Intern Med. 1967; 67 (July)Crossref PubMed Scopus (168) Google Scholar, 4Fulton CG An analytical study of confiscated samples of narcotic drugs.Int Microfilm J Legal Med (Fall). 1965; 1Google Scholar found small amounts of narcotic in samples of seized heroin (0-5 percent) which presumably caused the acute reaction, thus arguing against overdosage in those instances. Thus, there may not be a direct correlation between the severity of the end results and the amount of heroin taken, as there is with overdosage of morphine and other alkaloids. As noted in the article, pulmonary edema is almost universally found at autopsy in patients with heroin overdose, or what Helpern calls “acute reaction” to heroin, and it seems likely that the same mechanisms may operate for the clinical syndrome of “heroin pulmonary edema.” There are currently studies in progress here to clarify whether some cases of heroin pulmonary edema at least, may be due to a hypersensitivity-like reaction, or some other mechanism not involving simple overdose.

Types of Shock-Like Reaction During Transurethral Resection and Relation to Acute Renal Failure

Types of Shock-Like Reaction During Transurethral Resection and Relation to Acute Renal Failure

Toxic Symptoms Accompanied by Hemolysis During Transurethral Prostatectomy

No AccessJournal of Urology1 Mar 1948Toxic Symptoms Accompanied by Hemolysis During Transurethral Prostatectomy1 Miles Griffin Miles GriffinMiles Griffin More articles by this author View All Author Informationhttps://doi.org/10.1016/S0022-5347(17)69394-7AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail © 1948 by The American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetailsCited ByO’Donnell P (2018) Acid Phosphatase Elevation with Symptoms Following Transurethral Prostatic ResectionJournal of Urology, VOL. 131, NO. 4, (684-686), Online publication date: 1-Apr-1984.Ceccarelli C and Smith C (2018) Studies on Fluid and Electrolyte Alterations During Transurethral Prostatectomy: IIJournal of Urology, VOL. 86, NO. 4, (434-441), Online publication date: 1-Oct-1961.Ceccarelli F and Mantell L (2018) Studies on Fluid and Electrolyte Alterations During Transurethral Prostatectomy: IJournal of Urology, VOL. 85, NO. 1, (75-82), Online publication date: 1-Jan-1961.Hoyt H, Goebel J, Lee H and Schoenbrod J (2018) Types of Shock-Like Reaction During Transurethral Resection and Relation to Acute Renal FailureJournal of Urology, VOL. 79, NO. 3, (500-506), Online publication date: 1-Mar-1958.Conger K and Karafin L (2018) A Study of Irrigating Medium Extravasation During Transurethral SurgeryJournal of Urology, VOL. 78, NO. 5, (633-643), Online publication date: 1-Nov-1957.Harrison R, Boren J and Robison J (2018) Dilutional Hyponatremic Shock: Another Concept of the Transurethral Prostatic Resection ReactionJournal of Urology, VOL. 75, NO. 1, (95-110), Online publication date: 1-Jan-1956.Maluf N, Boren J and Brandes G (2018) Absorption of Irrigating Solution and Associated Changes Upon Transurethral Electroresection of ProstateJournal of Urology, VOL. 75, NO. 5, (824-836), Online publication date: 1-May-1956.Nicolai C and Cordonnier J (2018) Serum Electrolyte Changes During Transurethral Prostatic ResectionsJournal of Urology, VOL. 74, NO. 1, (118-122), Online publication date: 1-Jul-1955.Griffin M, Dobson L and Weaver J (2018) Volume of Irrigating Fluid Transfer During Transurethral Prostatectomy, Studied with RadioisotopesJournal of Urology, VOL. 74, NO. 5, (646-651), Online publication date: 1-Nov-1955.Hagstrom R (2018) Studies on Fluid Absorption During Transurethral Prostatic ResectionJournal of Urology, VOL. 73, NO. 5, (852-859), Online publication date: 1-May-1955.Creevy C (2018) The Mortality of Transurethral Prostatic ResectionJournal of Urology, VOL. 65, NO. 5, (876-882), Online publication date: 1-May-1951.Credle W, Warren H and Vest S (2018) Use of Urea Solutions as Irrigating FluidsJournal of Urology, VOL. 65, NO. 6, (1065-1074), Online publication date: 1-Jun-1951.Goodwin W, Cason J and Scott W (2018) Hemoglobinemia and Lower Nephron Nephrosis Following Transurethral Prostatic SurgeryJournal of Urology, VOL. 65, NO. 6, (1075-1092), Online publication date: 1-Jun-1951.Garske G, Phares O and Sweetser T (2018) The Status of Irrigating Fluids for Transurethral Resection: Our Experience and A Survey of the Use of Various Solutions By OthersJournal of Urology, VOL. 62, NO. 3, (322-327), Online publication date: 1-Sep-1949. Volume 59Issue 3March 1948Page: 431-436 Advertisement Copyright & Permissions© 1948 by The American Urological Association Education and Research, Inc.MetricsAuthor Information Miles Griffin More articles by this author Expand All Advertisement PDF DownloadLoading ...

AGRANULOCYTOSIS IN CHILDHOOD

ACUTE agranulocytosis of the type described by Werner Schultz in 1922 is characteristically a disease of middle-aged women. Definite cases in childhood are rare, although other leukopenic and granulocytopenic conditions, without the clinical signs characteristic of the disease, are not uncommon. The fundamental lesion is a depression of the bone marrow which results in arrest of maturation or complete destruction of the granulated series of white blood cells. By definition, there is no disturbance of the red cells or platelets in cases of pure agranulocytosis. Three groups of granulocytopenic conditions have been differentiated according to etiology 1 : 1. The acute or the peracute form or the Schultz type, which is considered to be a shocklike allergic reaction of the bone marrow to a noxious agent. In many cases this agent has been recognized to be some drug containing the benzene ring, especially aminopyrine, but frequently it is unknown. 2. More

ALLERGIC PHENOMENA IN TUBERCULOUS KERATITIS

The words allergy and anaphylaxis seem to have lost their earlier sharp distinction of meaning. Many of the recent reports on protein reactions are somewhat confusing to the reader because of the uncertainty regarding the nature of the phenomena described. Indeed, Van Leeuwen,1Doerr and others have expressed the opinion that allergy and anaphylaxis are quite similar and may be only variations of one reaction. Richet, in 1902, was the first to use the term anaphylaxis, and described it as a shocklike reaction induced in an animal by the second injection of a protein to which it had been previously sensitized. The symptoms of the many reports subsequently published were chills, fever, collapse, prostration and sometimes death. In 1916, Cooke2introduced the term allergy to designate a number of conditions which show one common etiologic characteristic, namely, hypersensitiveness to proteins or other substances which are innocuous to