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San Juan. Marchand Russell A. Soler Zapata J. No se devuelven originales. Ejemplo: 1. Koppisch, E. Todr material de anun. In most of the common dermatoses, infection, inflammation and allergy. By virtue of its dual components Sterosan- hydrocortisone effectively combats all three factors.

References; 1 Lubowe, I. Tubes of 5 and 20 Gm. New York STH allergic or inflammatory flare-up! Side effects none. Duration of therapy: 10 weeks. Photos by M. Nierman, M. Ease of use: Celestone has simple-to-follow dosage schedules based on a single tablet strength, 0. Pa- tients may be switched easily from other corticosteroids to Celestone with proper dosage adjustments.

Bibliography: 1. Goldman, L. Gant, J. Frank, L. Hampton, S. Bukantz, S. Bedell, H. Schwartz, E. Kammerer, W. Cohen, A. Gordon, D. Abrahamson, I.

Dosage: usually 2 tablets every 12 hours; 2 tablets three or four times daily in severe infections. Supplied: mg. Albamycin as novobiocin calcium and mg. GOTAS, con mg. Dolor intenso que obliga a inmovilizar u hospitalizar al enfermo y tomar medidas radicales. BOX BO. The stools of both of these boys contained schistosome eggs with lateral spine. In Sambon named the schistosome, which had lateral- spined eggs that were passed only in the feces.

Schistosoma man- soni, in honor of Sir Patrick Manson. Soon afterwards, it was definitely proven that this schistosome belonged to a distinct species. Three species of pathogenic schistosome had been described, the S. Japonicum, and more re- cently a probable new species known as S.

Here in Puerto Rico and probably in the entire West Indies as well as in South America, schistosomiasis appears to be due ex- clusively to S.

Invest at ion When a person wades or bathes for the first time in infested waters of lakes or slow moving rivers or streams, he develops a dermatitis produced by the penetration of the cercariae. Skptikmbhe, ing lasts for 1 or 2 days and all traces of dermatitis disappear within a few days.

These symptoms consist of anorexia, nausea, vomiting, slight abdominal pain, mild diarrhea, fatigability, and malaise. Acute Toxemic Stage Af 'er a period of incubation that varies between three to eight weeks according to Pons, which is about the time when the worms have matured, migrated into the mesenteric veins, and begun to deposit their eggs, there is a sudden onset of fever usually accom- panied by a dry cough, urticaria, variable gastrointestinal symp- toms, a tender enlarged liver, and a palpable spleen.

There is usually moderate leucocytosis with a marked eosinophilia. X-rays films of the lungs often show patchy areas of bronchopneumonia as evidence of the migration of the worms through the lungs. This febrile stage lasts for about two or three weeks but may be shortened by the administration of Fuadin, tartar emetic, or other salts of antimonium.

Again another symptom-free period ensues. Some infected persons will probably never show any further signs of the disease, but others will develop intestinal symptoms that vary between mild discomfort and diarrhea to a clear-cut picture of dysentery alternating with constipation. Throughout the entire illness signs and symptoms of colitis remain as the most prominent feature or complaint. We would add another type, the cardiopulmonary.

They are the three phases of the same pathologic process. The differences are simply those of timing and of degree, rather than of kind. Intestinal Symptoms Pons in Puerto Rico, , found that initial egg extrusion into the intestinal canal occurs from 37 to 44 days after exposure VoL. The ova of the parasites deposited in the submucosa cf the colon, sigmoid, and rectum frequently give rise to colitis six to eight weeks after infection. During this period there is ab- dominal pain often, frequent stools containing blood and mucus and also lateral spined eggs in the feces.

In long standing cases, polypoid growths may be felt inside the sphincter ani or may be found in any portion of the colon as high as the sigmoid flexure but the small intestine is rarely, if ever, affected except in its low- er part. Tenderness over the cecum is frequently observed. Deposition of ova of the parasite in the appendix may occur and produce symptoms of subacute appendicitis.

The fundamental histopathologic unit of the disease is the pseudotubercle, developing about the ova. The development of pseu- dotubercles, according to Koppisch, is traced from the early stage of eosinophilic and polymorphonuclear response through that of an epithelioid cell nodule to the final healed fibrous body.

There are, in addition, chronic inflammatory changes leading ultimately to fibrosis, especially in the colon and liver. Hepalosplenic Type From the beginning, the disease is primarily hepatic and colonic. Pathologic changes are instigated mainly by the deposi- tion of ova in the tissues; in the colon this leads to colitis and in the liver, to cirrhosis, which is characteristically periportal in dis- tribution. Splenomegaly develops in part, at least, secondary to portal obstruction.

After the initial or single massive infestation or after numer- ous exposures to the cercariae, the patient may remain symptom- less for months or years or he may complain of gastrointestinal discomfort, of an occasional bout of diarrhea, or may be subject lo dysentery alternating with constipation.

He may consult the physician either because of his digestive disturbances or becausi his abdomen has enlarged and he feels weak, anorectic, and tired. An enlarged spleen and an enlarged left lobe of the liver are found ill physical examination. For months and years the entire liver and the spleen increase in size.

We have seen it fill almost the entire large and distended abdominal cavity. On the other hand, the liver cnilarges for several years and then tends to become gradually smaller as the fibrotic changes progress; in the later stages, it may recede beneath the costal border. Aso '. Septiembre, The anatomical picture of the schistosomal cirrhosis is dif- ferent from all other known types of cirrhosis of the liver. It consists of inflammation of the intrahepatic portal radicles; granulomas, intrahepatic thrombophlebitis, and peri- portal fibrosis.

As a rule, the inflammation does not invade the lo- liule and there is no hepatocellular necrosis. Bogliolo claims that the ana- tomical picture of clay-pipestem cirrhosis may be diagnosed by simple macroscopic examination. Schistosomiasis mansoni was found in The highest incidence oc- curred in the age group between 20 and 29 years. In 16 cases 5. There were 16 cases 5. Patients showing the hepatosplenic type of disease rarely develop jaundice; rarely die in hepatic failure but often die of hematemesis due to ruptured esophageal or gastric varices, while patients with portal cirrhosis may go readily into coma following hemorrhage.

Those with schistosomal cirrhosis can withstand re- iieated hematemesis with impunity. One patient who withstood VoL. The treatment of choice for bleeding esophageal varices due to portal hypertension is probably shunt surgery, especially porto- caval anastomosis.

They considered the possibility of an aggravation of pre-existing pulmonary lesions due to the opening of a large direct passage for parasitic ova from the intestine to the lungs. The risk, they say, must be weighed against the more immediate danger that the unoperated patient may die of exsanguination due to bleeding eso- phageal varices. Pulmonary Schistosomiasis In the early stages of Schistosomiasis mansoni, the signs of bronchitis! In later stages the anastomosis between the mesenteric portal veins and the vena cava become enlarged and permit eggs, even worms, to be carried to the lungs.

In cases of massive single infections or repeated severe reinfections, extensive pulmonary fibrosis and chronic cor pulmonale may be seen.

The chronic cor pulmonale and right sided heart failure may be explained in some cases by the presence, in the lungs, of numerous arteriovenous communications and right to left shunts in angiomatoid forma tions of bilharzial origin. The Schisto- soma mansoni ova, but rarely the worms, reach the pulmonary cir- culation from the intestine via the internal iliac veins and the portocaval anastomosis. The ova, as emboli, obstruct the pulmonary arterioles and initiate a tissue reaction outside the arteriolar wall which results in formation of a granuloma.

The vascular 'esions result from passage of ova through the arteriolar walls wilh re- Hoi..

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