Oral histoplasmosis associated with HIV infection: a comparative study.

OBJECTIVE: Histoplasmosis is a granulomatous fungal disease caused by Histoplasma capsulatum. The objective of the present paper was to describe the prevalence of oral histoplasmosis (OH) in two services from an endemic area in Argentina between 1991 and 2002 and to compare the clinicopathological profile of OH between HIV-positive and HIV-negative patients. METHODS: About 733 HIV+ (group A) and 14 260 patients (group B) were examined. Clinical diagnosis was confirmed by cytology, biopsy or culture. RESULTS: About 21 (3%) and 10 (0.07%) cases of OH were diagnosed in group A and B respectively. Most patients were male. A total of 90% of patients in group A were <45 years old whereas 70% of group B were more than 45 years old. Palate, gingiva and oropharynx were the most frequent locations. The importance of including histoplasmosis in the differential diagnosis of ulcerated oral lesions in immunocompromised patients was discussed.

Renal tubular acidosis and vasculitis associated with IgE deposits in the kidney and small vessels.

We report a woman with a history of allergies, polyuria, polydipsia, proteinuria, renal loss of electrolytes, renal tubular acidosis, nephrocalcinosis, and palpable purpura. A proximal defect was excluded by a normal bicarbonate reabsorption curve, and a distal tubular defect was shown because urine pH did not decrease to less than 6.4 despite ammonium chloride-induced systemic acidosis. Moreover, furosemide failed to improve urinary acidification. Urine-to-blood PCO(2) gradient was less than 14 mm Hg, although the urine bicarbonate level reached values as high as 89 mEq/L. Combining bicarbonate and neutral phosphate infusions increased the urine-to-blood PCO(2) gradient to only 20 mm Hg. These subnormal PCO(2) gradient values point to proton-pump dysfunction in the collecting tubule. Histological evidence of tubulointerstitial disease accompanied the tubular defects. The striking histological feature was the presence of immunoglobulin E (IgE) deposits in glomeruli, tubuli, and vessels. Concurrent with these findings, she had high serum IgE titers and CD23 levels. IgE antibodies from her serum were reactive against human renal tubuli, with binding to two regions that matched two different proteins present in cortex and medulla. One of these proteins corresponded to carbonic anhydrase II (31 kd); the second, to an unidentified protein that seems attached to cell membranes. We suggest that these IgE antibodies could have had a pathogenic role in this patient's glomerular, tubular, and small-vessel disease.

[Diagnosis and etiology of Barrett esophagus. Presence of gastrin secreting cells (G cells)]. / Diagnóstico y etiología del esofago de Barrett. Presencia de células secretoras de gastrina (G).

We present the patterns for the diagnosis, checking the clinical, radiological, endoscopical and histological data of 35 patients suffering from Barrett's Esophagus (BE) (columnar metaplasia lining the lower esophagus). The clinical characteristics are those of a severe esophagitis of long evolution, although metaplasia itself is asymptomatic, and its features depend on the inflammation degree. Radiology can bring out some data as GE reflux, hiatal hernia, ulcers or stricture, and perhaps double contrast may show any sign by means of which endobrachyesophagus (EBE) can be suspected. Endoscopy provides us with accurate data about EBE, ulcers, stricture and inflammation. Histology reveals the type of columnar metaplasia (junctional or cardial, gastric fundic, intestinal or specialized, or composite). Acquired or congenital etiology can be clarified by an immunohistochemical method, Peroxidase anti-Peroxidase (PAP), showing the presence of gastrin secretory cells (G cells) in the congenital cases.

Diagnóstico y etiología del esofago de Barrett. Presencia de células secretoras de gastrina (G). / [Diagnosis and etiology of Barrett esophagus. Presence of gastrin secreting cells (G cells)]

We present the patterns for the diagnosis, checking the clinical, radiological, endoscopical and histological data of 35 patients suffering from Barretts Esophagus (BE) (columnar metaplasia lining the lower esophagus). The clinical characteristics are those of a severe esophagitis of long evolution, although metaplasia itself is asymptomatic, and its features depend on the inflammation degree. Radiology can bring out some data as GE reflux, hiatal hernia, ulcers or stricture, and perhaps double contrast may show any sign by means of which endobrachyesophagus (EBE) can be suspected. Endoscopy provides us with accurate data about EBE, ulcers, stricture and inflammation. Histology reveals the type of columnar metaplasia (junctional or cardial, gastric fundic, intestinal or specialized, or composite). Acquired or congenital etiology can be clarified by an immunohistochemical method, Peroxidase anti-Peroxidase (PAP), showing the presence of gastrin secretory cells (G cells) in the congenital cases.