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ABSTRACTS OF PAPERS AT THE 88TH RESEARCH MEETING OF THE MEDICAL RESEARCH CENTRE OF BOMBAY HOSPITAL ON MONDAY, 9TH JULY, 2001, 2.30 PM SP JAIN CAFETERIA (CONVENOR DR. HL DHAR)
1.A CASE OF GENITAL TUBERCULOSIS
Paresh Pate, PB Pai Dhunghat
A rare occurrence of combination of tuberculous peritonitis, tuberculous endometritis and tuberculous endocervitis.
A 34 year old lady Gravida 2, para 1, live 1, abortion 1, with history of scanty menstruation and abdominal pain on and off since 7-8 months. Before 8 months she had normal menstruation after which she started getting irregular menstruation. She gets her menses every 25-30 days, lasting for 1-2 days with very scanty flow. She has one full term normal delivery of a female child, 8 year old and 1 missed abortion for which dilatation and curettage was done.
No history of preceding menorrhagia. No history of tuberculosis/tuberculous contact in past/thyroid disorder/diabetes mellitus/hypertension/ischaemic heart disease.
On general examination she was averagely built and nourished with no pallor, icterus, cyanosis or lymphadenopathy.
Thyroid RS and breast CVS was normal.
Respiratory and cardiovascular systems showed no abnormality. Per abdomen examination showed mild tenderness all over abdomen. Per speculum examination showed cervical erosion on the anterior lip. Per vaginal examination showed normal sized uterus with mild tenderness in the fornices.
After admission, she was routinely investigated and found to be normal. Then the patient was subjected to hysteroscopy and laparoscopy. Hysteroscopy showed stenosed cervical canal and unhealthy endometrium with fibrosis.
Laparoscopy showed inflamed uterus, right lateral hydrosalpinx and left tubo ovarian mass and pouch of douglas omental adhesions.
Peritoneal biopsy was taken from 3 sides and sent for histopathology examination. Cervix biopsy was taken and sent for histopathology examination.
Histopathology report showed tuberculous peritonitis, tuberculosis endometritis with no atypia/malignancy.
2. HYPEROXALURIA
Suvarna Bhingarde, BN Apte
Hyperoxaluria in humans may result from genetic metabolic disease or may be acquired. The acquired hyperoxaluria is caused by pyridoxine deficiency or increased ingestion of oxalate or increased intake of the precursors. The hyperoxaluria resulting from the genetic cause is rare and is known as primary hyperoxaluria. It is divided into two types - Type I and Type II. Hyperoxaluria type I, typically occurs in young children, who have symptoms of renal colic and who develop calcium - oxalate nephrolithiasis. The affected children may develop growth retardation, uraemia and often succumb before the age of 20 years. Patients excrete quantities of glyoxylate, oxalate and glycolate.
A second rare from of hyperoxaluria has been reported to occur in children. This is known as hyperoxaluria type II. The children in this disorder suffer from glyceric aciduria and develop nephrocalcinosis, urolithiasis and the consequences of renal disease with growth failure and uraemia. Patients with this disease excrete large amounts of oxalates and glyceric acid in urine.
Both hyperoxaluria type I and type II are inherited as autosomal recessive traits.
We present here 3 cases of primary hyperoxaluria Type I, who were diagnosed and are being managed and followed up for the last several years.
3. METHYLMALONIC ACIDAEMIA
Suvarna Bhingarde, BN Apte
Methylmalonic acidaemia is a disorder which is characterized by profound metabolic ketoacidosis and developmental retardation with accumulation of huge amounts of methylmalonate in blood and urine.
A hereditary form of methymalonic aciduria is associated with the defect in methylmalonyl CoA racemase apoenzyme, methylmalonyl CoA mutase and the synthesis of adenosyl cobalamine. Primary defect in the synthesis of adenosyl cobalamine consequently leads to impaired mutase activity.
There are 3 distinct defects in the synthesis of adenosyl cobalamine-two which interfere with the synthesis of adenosyl cobalamine only and one that prevents the formation of both methyl cobalamine and adenosyl cobalamine.
Methylmalonic aciduria may also result from acquired Vitamin B12 deficiency. But the amount of Methylmalonic acid excreted in urine is low as compared to that found in urine of patients with the disease of genetic origin.
Methylmalonic acidaemia may be classified as Vitamin B12 responsive and non-responsive. Patients with methylmalonate CoA racemase or methylmalonate mutase deficiency are non-responsive to Vitamin B12. These patients can be managed on low protein diet.
However, methylmalonic acidaemia resulting from the defective synthesis of adenosyl cobalamine is Vitamin B12 responsive.
4. AN INTERESTING CASE OF ECTOPIC PREGNANCY
Nitin P Pai Dhunghat, PB Pai Dhunghat
1. No period of Amenorrhoea.
2. Managed with Therapeutic Laparoscopy.
A second gravida consulted with complaints of dull aching lower abdominal pain and referred by GP as an acute abdomen.
She was well educated and was absolutely certain that she had not missed a period, her last period was on 6.6.2001.
However, it did come 10 days late and hence she had urine pregnancy test done which was negative on 4.6.2001.
She had one previous normal delivery of a male child 2 years ago.
On clinical examination, she was stable with BP of 130/80 mm of Hg., pulse 100/min and minimal pallor.
However per abdominal examination revealed lower abdominal tenderness.
Per vaginal examination also revealed tenderness in the posterior fornix along with tender cervical movements and posterior fornix bogginess. An urgent USG revealed a large haematoma in the posterior fornix.
After arranging for Blood a Therapeutic laparoscopy was done. A thorough wash with irrigation was given.
The wash seemed to contain Tubal abortus. The tube and ovaries looked normal. But on closer inspection the right fimbrial end was bleeding actively and hence was cauterised. At the time of first post operative visit the patient was alright and histopathology confirmed diagnosis of tubal abortion. Serum BHCG was less than 10.
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