pouch were dissected away. The head of the tibia was found covered with more or less fibrous tissue. The semilunar cartilages seemed to be intact and not hypermobile. Both wounds were closed with fine silk in layers, subcutaneous catgut sutures and skin sutures of silk. The knee was immobilized in a heavy dressing, cotton rollers and a com¬ press bandage. The operation was done under the tourniquet. The pathologist reported a cavernous hemangioma apparently removed intact.The patient had a normal convalescence ; the stitches were removed on the seventh day. In May, 1925, the patient reported that she was free from all symptoms, using the knee without discomfort, and had had no return of trouble. CONCLUSIONS 1. In the diagnosis of "internal derangements" of the knee joint, the presence of hemangioma must be excluded, especially if the history indicates a long stand¬ ing disability or one resulting from trauma.2. It is most frequently found in children and young adults.3. Adequate roentgen-ray and radium treatment should be given before operative intervention is considered.4. The prognosis should be guarded. 5. Careful observation over a long period, after any form of treatment, should be insisted on.
The diagnosis of Bartter syndrome was established in a 21 year old female patient, who presented with hypokalaemia and hyperkaluria, alkalosis, hyperreninism, hyperaldosteronism, and decreased fractional chloride reabsorption in the ascending limb of Henle's loop.Her stature was very short (140 cm) with otherwise normal body proportions. At birth, a coloboma of the right eye, dislocation of the left hip, and syndactyly of the second and third toes of the right foot were present. Since the age of 13, -she has suffered from recurrent attacks of gouty arthritis. At the age of 20, she presented with hyperglycaemia and glucosuria for which she had received insulin for one year. Family investigations revealed consanguinity between the parents (F=1/256).Karyotyping was first performed at the age of two, and showed trisomy 3 in 10% of leucocytes. At the age of 21, another cytogenetic evaluation was performed which revealed mosaicism for a normal and a trisomic cell line. In cultured blood leucocytes, a 47,XX,+3 karyotype was found in the majority of mitoses. In all cultivated skin fibroblasts, however, the karotype was 46,XX.Whether there is a causal relationship between trisomy 3 and Bartter syndrome is unknown. This association has not been reported before.Trisomy 3 is very rare in liveborn children. A case of trisomy 3 mosaicism was reported in a female baby who presented with severe failure to thrive and died at the age of five months.' She had a 47,XX, +3 complement in leucocyte cultures, but showed a normal 46,XX karyotype in skin fibroblasts. The baby had a large skull, low set, malformed ears, and
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