Adobe Scan Apr 20, 2024
Adobe Scan Apr 20, 2024
Adobe Scan Apr 20, 2024
Procedure:
Fusion PET/CT imaging was pertormed on uMI 550 digital PET-CT system from the head to toes 102 mins after IV
administration of 5.04 mCi of F-18 fluorodeoxyglucose (FDG). Contrast-enhanced CT was performed for the
Durpose of attenuation correction and anatomical correlation. Sr. Creatinine level was 0.9 mg/dl (02/04/2024).
Blood glucose level was 106 mg/dl prior to scan. SUV values, wherever mentioned, have been measured in gm/ml.
Note: All tumors are not FDG avid. In the absence of metabolically active disease reported on the scan, if there are other evidences to suggest
presence of disease, complimentary investigations should be undertaken. Investigations have their limitations. Solitary pathol ogical/ radiological
and other investigations never confirm the final diagnosis of disease. They help in diagnosing the disease in correlation to clinical symptoms &
other related tests. Please interpret accordingly.
FDG PET/CT is not a sensitive modality for brain metastases, consider MRI brain if clinically indicated.
Head &Neck:
Physiological FDG uptake is noted in the head and neck.
No significant FDG avid cervical or supraclavicular nodes are seen.
Thorax:
No pleural or pericardial effusion seen.
No significant FDG uptake is noted in the lungs.
Increased FDG uptake is seen in the subem-sized subcarinal node (SUVmax 5.8) - likely inflammatory.
No significant FDG-avid axillary or hilar nodes are seen.
Page 1 of 2
Extremities:
No demonstrable
abnormal FDG uptake noted in both the lower limbs.
OPINION
H/o slurring of speech, for evaluation.
No significant metabolically active disease anywhere in the whole-body survey.
Maeyan
DR. SHREYAS KUDACHI
MBBS, DRM, Masters in Oncologic Imaging
Consultant, Nuclear Medicine & PET-CT
Page 2 of 2
Discharge Summary
Patient Name ANANDA JAGANNATH JADHAV
Diagnosis:
SUBACUTE DYSARTHRIA
UNPROVOKED LAUGHTER
LEFT UPPER LIMB PROXIMAL WEAKNESS WITH FASCICULATIONS
?MND.
****
Presenting Illness:
A S3 YEARSs OLD MALE PATIENT ADMITTED WITH DIFFICULTY IN SPEAKING, LEFT UPPER LIMB
WEAKNESs, SLOWNESS OF ACTIVITIS, TWITCHING OVER LEFT UPER LIMB.
Past History:
NOT A CASE OF DM/HTN/IHD
HO.- PATIIENT CONSULTED WITH DR.KEDARI PRASAD KULKARNI SIR, INVESTIGATIONS DONE
1) CBC/RFT/BSL/TSH -NORMAL , HIV- NEGATIVE
2) TOTAL PROTEIN - 7.8, ALBUMIN- 4,4
3) IPTH -21 (15-65 NORMAL)
4) PROTEIN ELECTROPHORESIS - MONOCLONAL BAND NOT SEEN
5) NCS (5/2/2024) B/L ? ANT. MOTOR AXONOPATHY IN UPPER AND LOWER LIMB. ?ANT. HORN CELL
DISEASE.
6)MRI BRAIN (15/1/2024)- ISCHEMIC CHANGES IN B/L FRONTO-PARITAL WHITE MATTER.
Course in Hospital:
A MALE PATIENT ADMITTED WITH ABOVE MENTIONED COMPLAINTS. AFTER INITIAL ASSESSMENT
ALL NEEDED INVESTIGATIONS DONE.
DIAMOND SUPERSPECIALITY HOSPITAL
(A Venture of Kolhapur Super-Speciality Medical Centre)
184/1,Near Acharya Vidyanand Bhavan, 'e Ward,
Nagala Park kolhapur416002. Ph:0231-2667044/45/46,2668811,2667244.
ANYWHERE INN
PET SCAN DONE ON 3/4/2024 NO SIGNIFICANT METABOLICALLY ACTIVE DISEASE
WHOLE BODY SURVEY.
PATIENT CLINICALLY AND SYMPTOMATICALLY STABLE HENCE DISCHARGED WITH STABLE VITALS.
Treatment Given
TREATMENT GIVEN
INJ NERVZ/ ELDERVIT/THIAMINE IV OD 3 DAYS
INJ PAN 40MG STAT AND OD
INJ EMSET 4MG IV STATAND TID
TAB Q-NENS 500MG OD
CAP EVION 400MG HS
TAB RILUTOR 50MG HS
Remark
Treatment Advice
Medicine Name Drug Name Mor Eve Days Spl.Instruction
TABQNENS 500 MG
CAP EVION 400 MG
TAB RILUTOR 50 MG
CAP OMELIFE 20 MG
Remark:
F/U WITH DR AURANGABADKAR SIR AFTER 5 DAYS.
aeoineeiane
Issue:
Mr. ANANDA JAGANNATH JADHAV Reference: DR.KAUSTUBH
Medical Laboratory Report
VID: 240087100143691
KOP Karveer.. AURANGABADKAR
Tel No 9999900000 Sample Collected At: Registered On:
Maxcare Lab 04/04/2024 08:31 PM
PID NO: P18824521451308
Mahalaxmi Apartment Gala No 203 Collected On:
Age: 53 Year(s) Sex: Male Rajarampuri 2nd Lane Kolhapur. 04/04/2024 8:14PM
Processing Location:- Metropolis Reported On:
Healthcare Ltd,Unit No409-416,4th
Floor, Commercial EBuilding-1,Kohinoor 05/04/2024 04:20 PM
Mall, Mumbai-70
Acetyl Choline Receptor Autoantibodies is highly specific for the diagnosis of Myasthenia Gravis (MG).
in the majority of patients (-85%) antibodies against the muscle acetylcholine receptor (AChR) are detected, while 6%
antibodies against the muscle-specific kinase (MuSK) are detected.
In approximately 10% of MG patients no autoantibodies can be found with the classical diagnostics for AChR and MuSK
antibodies
The antibody titres be
can negative or not detectable in the first 12 months after the onset of symptoms of MG or during
immunosuppressant therapy.
The magnitude of the antibody titres correlates poorly with severity of MG and hence is not useful for predicting disease
activity.
Note:-. Positivity is observed in a few cases post covid due to molecular mimicry.
Associated Test: Musk Antibody (M0080)
References-
Vincent A, Newsom-Davis J. Acetyicholine receptor antibody as a diagnostic test for myasthenia gravis: resuits in 153
validated cases and 2967 diagnostic assays. J Neurol Neurosurg
Psychiatry 1985; 48: 1246-52.
Limberg PC, Hummel E, Relationship between changes in anti-acetylcholine receptor antibody concentration & disease
severityin myasthenia gravis. Ann NY Acad Sci 1981; 377: 859-61.
Garlepp MJ, Kay PH, Dawkins RL. The diagnostic significance of auto antibodies to the acetylcholine receptor. J
Neuroimmunol 1982; 3:337-50.
Muralidhar Reddy Y, B SK, Osman S, et alTemporal association between SARS-CoV-2 and
new-onset myasthenia gravis:
is it causal or coincidental?BMJ Case Reports CP 2021;14:e244146.
Lazaridis K, Tzartos SJ. Autoantibody Specficities in Myasthenia Gravis,
Implications for Improved Diagnostics and
Therapeutics. Front Immunol, 2020 Feb 14;11:212
Kit Insert
--
End of Report
Tests marked with NABL symbol are accredited by NABL vide Certificate no MC-2139; Validity till 01-06-2024
Page 1 of 1
Dr. ALAP CHRISTY
Head
MBBS, MD, PGDM-HC
-
Acetyl Choline Receptor Autoantibodiesis highly specific for the diagnosis of Myasthenia Gravis (MG).
inthemajority of patients (-85%) antibodies against the muscile acetylcholine receptor (AChR) are detected, weile %
antibodies against the muscle-specific kinase (MusK) are detected.
Inapproximately 10% of MG patients no autoantibodies can be found with the dlassical diagnosics for AChR and MsK
antibodies
The antibody titres can be negative or not detectable in the first 12 months after the onset of syrmptoms cf MGr during
immunosuppressant therapy.
The magnitude of the antibody titres corelates poorly with severity of MG and hence is not useful for predicting disease
activity.
Note:- Positivity is observed in a few cases post covid due to molecular mimicy.
References-
Vincent A, Newsom-Davis J. Acetylcholine receptor antibody as a diagnostic test for myasthenia gravis: resuts in 153
validated cases and 2967 diagnostic assays. J Neurol Neurosurg Psychiatry 1985; 48: 1246-52.
Limberg PC, Hummel E, Relationshipbetween changesin anti-acetylcholine receptor antibody concentration &disease
severity in myasthenia gravis. Ann N Y Acad Sci 1981; 377: 859-61.
Garlepp MJ, Kay PH, Dawkins RL. The diagnostic significance of autoantibodies to the acetylcholine receptor. J
Neuroimmunol 1982; 3: 337-50.
Muralidhar Reddy Y, B SK, Osman S,etalTemporalassociation between SARS-CoV-2 and new-onset myasthenia gravis
is it causal or coincidental?BMJ Case Reports CP 2021;14:e244146.
Lazaridis K, Tzartos SJ. Autoantibody Specificities in Myasthenia Gravis, Implications for Improved Diagnostics and
Therapeutics. Front Immunol, 2020 Feb 14;11:212
Kit Insent
-- End of Report --
Tests marked with NABL symbol are accrodited by NABL vide Certificate no MC-2138; Validitysll01-06-2024
Page 1 of1
End Of Report-
UREA CREATININE
Test Result Unit Biological Ref. Range
S. Creatinine 0.90
Method: Jafe's Kinetic mg/d 0.7-1.2 mg/dl
(Collected At: 02/04/2024 20:26:42, Received At: 02/04/2024 20:26:42, Reported At: 03/04/2024 07:48:13)
CPK (TOTAL)
Test Result Unit Biological Ref. Range
(Collected At: 02/04/2024 20:26:42, Receved At: 02/04/2024 20:26:42, Reported At: 02/04/2024 23:2744)
End Of Report
PATHOLOGY REPORT
80 020924
LAB ID :80 Sample Collection: 02/04/2024 20:26
Name : MR. ANANDA JAGANATH JADHAV Age 53 Yrs. Sex: M Sample Received :02/04/2024 20:26
Ref. By: DR. KAUSTUBH AURANGABADKAR :02/04/2024 23:27
Printed :03/04/2024 10:11 Report Released
Sent By: Direct
Primary mafunction of thyroid gland may result in excessive (hyper) or below normal (hypo) release of T3 or T4. In addition, as TSH directly affects
thyrold function, malfunctin of pituitary or the hypothalamus influences the thyrold gland activity. Disease of any portion the thyroid-pituitary-
blood.
hypothalamus system may influence the levels of T3 and T4 in the
TSH (ulUml)
| FOR PREGNANT WOMEN T3(ng/di) T4 (ng/d )
0.0878-2.8
1 st TRIMESTER 81.1-176.6 5.61-13.3
7.3614.18 0.1998-2.8
2 nd TRIMESTER 92.8-205.1
0.307-2.9
3 rd TRIMESTER 90.9-205.1 | 7.37-15.02
ET T TETZ fundamentals of clinical chemistry 2. guidlines of the American thyroid association durling pregnancy and postpartum, 2011.
End Of Report
PET-e
- P U Y s i oTCERAHY
COnsult Dy
banugade e 1 TSH
Kiqr
-1
moniis CBCTFT
T QNENS (SUO)
-X